Reported by (76)
Vasoactive substances as mediators of renal injury
2018, Comprehensive Toxicology: Third Edition
Kidney function is regulated by a complex interplay between circulating and locally produced chemicals called vasoactive substances. These substances affect the tone of the renal vessels, causing either vasodilation or vasoconstriction. and consequently affect renal blood flow and/or glomerular filtration rate. They belong to a chemically heterogeneous group and include proteins, peptides, lipids and nucleosides. This chapter summarizes the role of these vasoactive substances in maintaining normal renal function and also highlights their role in diseases such as acute kidney injury, chronic kidney disease, and hypertension.
The growing role of eicosanoids in tissue regeneration, repair and wound healing
2013, Prostaglandins and other lipid mediators
Citatuddrag:
This has been tested elsewhere [79,80]. Specifically, eicosanoids play a role in regulating renal blood flow and glomerular filtration rate [81,82]. However, the role of eicosanoids in kidney repair and regeneration is not well characterized.
Tissue repair and regeneration are essential processes to maintain tissue homeostasis, particularly in response to injury or stress. Eicosanoids are ubiquitous mediators of cell proliferation, differentiation, and angiogenesis, all of which are important for tissue development. Eicosanoids modulate the initiation and resolution of inflammation associated with the tissue response to injury. In this Review, we describe how this diverse group of molecules is an important regulator of tissue repair and regeneration in multiple organ systems and biological contexts.
Endothelial control of vasomotor tone: The renal perspective
2012, Nephrology Seminars
Citatuddrag:
Although originally thought to be only an endocrine regulatory system for blood pressure, it is now generally accepted that it also acts in a paracrine/autocrine manner.33 With the sequential description of arachidonic acid derivatives, NO, endothelin and other vasoactive lipids and the evidence that these Substances can be synthesized by the kidneys (Table 1).34–38 It has been suggested that increased renal synthesis of vasoconstrictor metabolites or decreased production of renal vasodilators may be involved in the development of hypertension. However, it is currently believed that most of these substances synthesized in the kidney act mainly as local metabolites, with their systemic effects being less relevant.
(Video) Pharmacology - NSAIDs & PROSTAGLANDIN ANALOGS (MADE EASY)Endothelial cells are key regulators of vascular tone. They do this by sensing humoral mediators and transmitting their effects to the underlying vascular smooth muscle, as well as by synthesizing vasoactive molecules that act paracrinely. In the kidney, the local release of these endothelial mediators together with the accumulation of specialized endothelial cells in the glomerulus contribute to the regulation of renal blood flow, glomerular filtration, and tubular function, which are closely related to sodium balance as they mutually influence each other. . Ultimately, renal circulation and tubular function have a significant impact on systemic blood pressure due to the overall regulation of volume homeostasis.
Analgesics and non-steroidal anti-inflammatory drugs
2010, Comprehensive Toxicology, Second Edition
Nonsteroidal anti-inflammatory drugs (NSAIDs) are relatively safe and effective chemicals used for pain, inflammation, and fever. All NSAIDs inhibit the enzymes responsible for the synthesis of prostaglandins. The most common side effects of NSAID treatment affect the gastrointestinal tract. However, some patients may experience side effects related to kidney function. These effects can range from relatively mild salt and water retention to acute tubular or chronic papillary necrosis. Side effects of NSAIDs affecting kidney function are the focus of this chapter.
Vasoactive substances as mediators of renal injury
2010, Comprehensive Toxicology, Second Edition
Kidney function is regulated by a complex interplay between circulating and locally produced chemicals called vasoactive substances. These substances affect the tone of the renal vessels, causing either vasodilation or vasoconstriction. and consequently affect renal blood flow and/or glomerular filtration rate. They belong to a chemically heterogeneous group and include proteins, peptides, lipids and nucleosides. This chapter summarizes the role of these vasoactive substances in maintaining normal renal function and also highlights their role in diseases such as acute kidney injury, chronic kidney disease, and hypertension.
Physiological and pathophysiological role of lipid mediators in the kidney
2007, Kidney International
Citatuddrag:
It has long been known that COX-derived prostanoids play a critical role in the regulation of renal blood flow (RBF) and glomerular filtration rate (GFR).74-76 Under normal conditions, prostanoids appear to have little effect on RBF and in GFR. .74 However, maintenance of normal renal function is dependent on prostanoids under certain pathophysiological conditions, particularly volume contractions such as heart failure, cirrhosis with ascites, and nephrotic syndrome.75-78
(Video) Anti-inflammatory (NSAIDs) Drugs, Pharmacology, AnimationSmall lipids such as eicosanoids perform diverse and complex functions. In addition to their role in regulating normal kidney function, these lipids also play an important role in the pathogenesis of kidney disease. Cyclooxygenase (COX)-derived prostanoids play an important role in maintaining renal function, body fluid homeostasis, and blood pressure. COX2-derived prostanoids from the renal cortex, in particular (PGI2) and PGE2, play a critical role in maintaining blood pressure and renal function in states of volume contraction. COX2-derived prostanoids from the renal medulla appear to have antihypertensive effects in subjects exposed to a high-salt diet. 5-lipoxygenase (LO)-derived leukotrienes are involved in inflammatory glomerular damage. The LO product 12-hydroxyeicosatetraenoic acid (12-HETE) is associated with the pathogenesis of hypertension and may mediate angiotensin II and TGFsiinduced mesenchymal cell abnormality in diabetic nephropathy. P450 hydroxylase-derived 20-HETE is a potent vasoconstrictor and is involved in the pathogenesis of hypertension. P450-derived epoxyeicosatrienoic acids (EETs) have vasodilatory and natriuretic effects. Blockade of EET formation is associated with salt-sensitive hypertension. Ceramide has also been shown to be an important signaling molecule involved in the pathogenesis of acute kidney injury from ischemia/reperfusion and toxic insult. These pathways should be fruitful targets for interventions in the pharmacological treatment of kidney disease.
Featured Articles (6)
research article
Impact of aging on renal function and monitoring and support
Surgical Clinics of North America, Band 95, Ausgabe 1, 2015, s. 71-83
research article
Evaluation of susceptibility to ionophores Eimeria acervulina and Eimeria maxima isolated from poultry farms in Algeria to Jijel province
Veterinary Parasitology, volume 224, 2016, pp. 77-81
This study represents the first description of ionophore resistance in animals obtained from commercial broiler farms of Algeria (Jijel-Algeriet). Microscopy and intermediate transcribed sequencing 1-PCR (ITS1-PCR) revealed only 2EimeriaSpecies found in waste from these operations – e.gmDatepileAndmDateMaxima. A panel of these isolates was tested in broiler chickens (Cobb 500) for susceptibility to five anticoccidial compounds: diclazuril (1 ppm), lasalocid (125 ppm), monensin (125 ppm), narasin (70 ppm), and salinomycin (60 ppm). Complete resistance to monensin and narasin, partial resistance to salinomycin and lasaloside, and complete susceptibility to diclazuril were observed, as indicated by anticoccidial susceptibility profiles based on lesion score and anticoccidial index (ACI). Although the lack of sensitivity to monensin is not surprising given that it has been used as the only anticoccidial compound for years, resistance to the monoether (Narasin) and ionophore polyethers (Lasalocid) suggests that a portion of monensin has developed cross-resistanceEimeriaPopulation. The beautiful uniformEimeriaThe species composition of all poultry farms indicates thisE. pileAndE. Maximadevelop resistance to ionophore drugs more quickly.
(Video) NSAIDs and Renal Functionresearch article
The effect of composting on the persistence of four ionophores in dairy manure and poultry litter
Waste Management, Volume 54, 2016, pp. 110-117
Manure composting is a well-described approach to stabilize nutrients and reduce pathogens and odors. Although composting studies have shown that thermophilic temperatures and aerobic conditions can increase the rate of removal of selected antibiotics, comparable information is lacking for many other compounds in untreated or composted manure. The objective of this study was to determine the relative effectiveness of composting conditions in reducing the levels of four commonly used ionophoric feed additives in dairy manure and poultry litter. Duplicate samples of fresh poultry manure and dairy manure were supplemented with 10 mg/kg monensin, lasaloside, salinomycin, or ambrolium−1DW. Samples of unmodified and modified dairy manure and poultry litter were incubated at 22, 45, 55 or 65°C under moist, aerobic conditions. Residue levels were determined from fractions taken at 1, 2, 4, 6, 8 and 12 weeks. The results indicate that the effectiveness of composting in reducing pollution is component and matrix specific. Composting temperatures were not more effective than ambient temperature in either poultry litter or dairy manure in increasing the rate or extent of monensin removal. Composting was effective in removing lasalocid from poultry litter, but is probably too slow to be practical (8-12 weeks at 65°C for >90% residue removal). Composting was effective in removing ambrolium from poultry litter and salinomycin in dairy manure, but in both cases it took 4-6 weeks to achieve >90% removal. However, composting did not increase the removal rate of salinomycin in poultry litter or the removal rate of lasaloside or ambrolium in dairy manure.
research article
Hyperphosphatemia induces cellular senescence in human aortic smooth muscle cells through upregulation of integrin-linked kinase (ILK).
Mechanisms of Aging and Development, bind 152, 2015, pp. 43-55
Aging is caused by genetic and environmental factors. Hyperphosphatemia is associated with certain pathologies that affect the behavior of vascular cells. This work analyzes whether a high concentration of extracellular phosphate induces the senescence of vascular smooth muscle cells, investigates the intracellular mechanisms, and sheds light on the in vivo relevance of this phenomenon.
Human aortic smooth muscle cells treated with β-glycerophosphate (BGP, 10 mM) underwent cellular senescence by increasing p53, p21, and p16 expression and senescence-associated β-galactosidase activity. In parallel, BGP induced ILK overexpression dependent on IGF-1 receptor activation and oxidative stress. Downregulation of ILK expression prevented BGP- and oxidative stress-induced senescence. Aortic rings from young rats treated with 10 mM BGP for 48 h showed increased p53, p16, and ILK expression and SA-β-gal activity. Seven/eight nephrectomized rats fed a hyperphosphatemic diet and fifteen-month-old mice showed hyperphosphatemia and aortic ILK, p53, and p16 expression.
In conclusion, we have shown that high extracellular phosphate induces senescence in cultured smooth muscle through IGF-1 receptor activation and ILK overexpression, and provide strong evidence of the in vivo relevance of these results, as aged animals had high serum phosphate overexpression of ILK and senescence genes.
(Video) Pharmacology - Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)research article
Airway exacerbations in native children from two countries with non-cystic fibrosis, chronic suppurative lung disease/bronchiectasis
Chest, Volume 146, Issue 3, 2014, pp. 762–774
Acute respiratory exacerbations (AREs) result in morbidity and deterioration of lung function in children with chronic suppurative lung disease (CSLD) and bronchiectasis. In a prospective longitudinal cohort study, we identified patterns of AREs and factors associated with increased risk of AREs in children with CSLD/bronchiectasis.
93 Indigenous children aged 0.5 to 8 years with CSLD/bronchiectasis in Australia (n=57) and Alaska (n=36) in 2004–2009 were followed for >3 years. Standardized parent interviews, physical examinations, and medical record reviews were conducted at enrollment and every 3 to 6 months thereafter.
93 children experienced 280 AREs during the 3-year period (median = 2, range = 0–11 per child). 91 (32%) were associated with pneumonia and 43 (15%) resulted in hospitalization. Of the 93 children, 69 (74%) experienced more than two AREs over the three-year period, and 28 (30%) had more than one ARE in each study year. The incidence of AREs decreased significantly with each year of follow-up. Factors associated with recurrent (two or more) AREs included age < 3 years, ARE-related hospitalization in the first year of life, and pneumonia or ARE hospitalization in the year before enrollment. Factors associated with hospitalization for acute respiratory illness in the first year of the study included age < 3 years, education of female caregivers, and regular use of bronchodilators.
AREs are common in children with CSLD/bronchiectasis, but with increasing clinical care and time, AREs occur less frequently. All children with CSLD/bronchiectasis require extensive care. However, treatment strategies for these patients may vary, depending on how the risk of AARE changes each year of treatment.
research article
Successful implantation and direct activation of vagus nerve stimulation (VNS) during pregnancy in a patient with intractable epilepsy: a case report and review of the literature
Journal of Clinical Neuroscience, Band 42, 2017, s. 114-115
While vagus nerve stimulation (VNS) has been shown to be a safe and effective adjunctive treatment in the general population for medically intractable seizures, little has been published about implantation during pregnancy. Here we present the case of a 21-year-old primiparous woman with medically refractory seizures who underwent safe and successful VNS implantation and immediate device activation at 32 weeks' gestation, resulting in dramatically improved seizure control and subsequent delivery of a healthy infant.
Copyright © 1986 Published by Excerpta Medica Inc.
FAQs
How do prostaglandins affect renal function? ›
Prostaglandins (PGs) with best-defined renal functions are PGE2 and prostacyclin (PGI2). These vasodilatory PGs increase renal blood flow and glomerular filtration rate under conditions associated with decreased actual or effective circulating volume, resulting in greater tubular flow and secretion of potassium.
What are the renal effects of non steroidal anti inflammatory drugs? ›NSAIDs reversibly inhibit the production of renal prostaglandins via their inhibition of COX-1 and COX-2. Maximal inhibition occurs at steady state plasma concentrations (usually 3–7 days). Renal prostaglandins cause dilatation of the renal afferent arteriole.
How do NSAIDs affect the kidney arterioles? ›NSAIDs, by inhibition of prostaglandins and bradykinin, produce vasoconstriction of the afferent renal arteriole and reduce the ability of the kidney to regulate (increase) glomerular blood flow.
How do NSAIDs decrease renal function? ›NSAIDs disrupt the compensatory vasodilation response of renal prostaglandins to vasoconstrictor hormones released by the body [5]. Inhibition of renal prostaglandins results in acute deterioration of renal function after ingestion of NSAIDs.
What happens when prostaglandins are increased? ›What happens if my levels of prostaglandins are too high? High levels of prostaglandins are produced in response to injury or infection and cause inflammation, which is associated with the symptoms of redness, swelling, pain and fever. This is an important part of the body's normal healing process.
How does prostaglandin effect potassium? ›The mechanisms by which prostaglandins pro- duce vasodilation are not known; the current data indicate that prostaglandins may induce relaxation of vascular smooth muscle by increasing the elec- trogenic transport of sodium and potassium by Na- K ATPase.
Which anti-inflammatory drug can cause renal failure? ›Heavy or long-term use of some of these medicines, such as ibuprofen, naproxen, and higher dose aspirin, can cause chronic kidney disease known as chronic interstitial nephritis.
How can NSAIDs cause kidney damage and high blood pressure? ›NSAIDs may increase your fluid retention and can lead to decreased blood flow to kidneys. This is because NSAIDs block prostaglandins, which are the natural chemicals that dilate blood vessels and allow oxygen to reach the kidneys to keep them alive and healthy.
Do NSAIDs decrease GFR? ›NSAIDs carry a risk of gradual decrease of GFR as well as acute kidney damage [10–13], and NSAID users without previous renal disorder had a three-fold greater risk for developing acute renal failure compared with non-NSAID users in the general population in United Kingdom [14].
Do NSAIDs affect renal blood flow? ›When the kidney is in a salt retaining state or when there is renal vascular damage, NSAIDs can reduce renal blood flow and glomerular filtration rate producing acute renal failure that is reversible upon discontinuation of the drug.
Do NSAIDs increase renal blood flow? ›
Nonsteroidal antiinflammatory drugs inhibit prostaglandin synthesis and cause a profound reduction in renal blood flow, with resultant kidney failure occurring in a high proportion of these patients.
Do NSAIDs cause vasoconstriction of afferent arteriole? ›NSAIDs block the vasodilatory effect of prostaglandins - UpToDate. Certain conditions that promote renal vasoconstriction and renal hypoperfusion require prostaglandins to vasodilate the afferent arteriole and blunt vasoconstriction to maintain a normal GFR (left).
How does ibuprofen affect the renal blood flow? ›Ibuprofen inhibits COX enzyme to reduce PG production so that the renal tubules contract, resulting in a decrease in renal blood flow (RBF), a decrease in glomerular filtration rate (GFR), and finally renal tubular toxicity (Li, 2001).
Do ACE inhibitors increase GFR? ›In general, ACE-inhibition does not affect normal glomerular filtration rate (GFR) but may increase GFR in patients on a low sodium intake prior to treatment. Since the rise in GFR is smaller than the rise in renal blood flow, in most instances a decrease in filtration fraction will result.
What are the four effects of prostaglandins? ›Prostaglandins can: Activate or inhibit (prevent) platelet buildup for blood clot formation. Cause vasodilation (widening of blood vessels) or vasoconstriction (narrowing of blood vessels). Cause bronchoconstriction (the narrowing of air passageways) or bronchodilation (widening of air passageways).
What is a negative effect of prostaglandins in the body? ›[9] Systemically administered prostaglandins are usually tolerated reasonably well, but there may be some side effects such as fever, hypotension, musculoskeletal pain, and cough.
What are the side effects of prostaglandins? ›Complications. Too many or too few prostaglandins in the body can cause health complications. Known problems with too many prostaglandins include arthritis and menstrual cramping. Conditions that can result from too few prostaglandins include glaucoma and stomach ulcers.
How does prostaglandin affect blood pressure? ›One of the most striking actions of prostaglandins of the E and A series is their capacity to dilate peripheral blood vessels and thereby to lower arterial pressure.
What is the most common adverse effect of prostaglandin analogues? ›These molecules all have similar side-effect profiles, which include both side effects that occur frequently (e.g., conjunctiva hyperaemia, increase of iris pigmentation and eyelash changes) and rare adverse reactions (e.g., periocular pigmentation, damage to the blood-aqueous barrier and cystoid macular oedema).
How do prostaglandins effect BP? ›A large body of evidence supports the concept that prostaglandins (PG) are importantly involved in arterial pressure regulation. Various PGs, especially PGE2 and prostacyclin (PGI2) may influence blood pressure through control of vascular tone, sodium excretion, and renin release.
Why are NSAIDs contraindicated in renal failure? ›
NSAIDs may also produce direct toxic effects on the kidney. The main mechanisms for acute renal failure include acute tubular necrosis and acute interstitial nephritis. Other rarer mechanisms have also been reported, such as acute papillary necrosis and renal vasculitis.
What drugs worsen renal function? ›Many drug classes cause renal insults. The top six classes were pain killers, antibiotics, proton pump inhibitors, antidiabetics, antihyperlipidemics, and agents for erectile dysfunction. Renal insults caused by these agents could vary in severity.
Is Tylenol or ibuprofen worse for your kidneys? ›Ibuprofen is harder on the kidneys than acetaminophen. Acetaminophen doesn't have the same effect on the COX pathway as ibuprofen. So kidney damage is much more rare. Kidney issues are typically only reported when a person has taken too much acetaminophen.
Can ibuprofen raise creatinine levels? ›Generally, an increase in serum creatinine concentrations is observed during treatment with ibuprofen, with a more pronounced effect during the early neonatal life, i.e., the first week of life.
What effect does inflammation have on GFR? ›Inflammation directly correlates with the glomerular filtration rate (GFR) in CKD and culminates in dialysis patients, where extracorporeal factors, such as impurities in dialysis water, microbiological quality of the dialysate, and bioincompatible factors in the dialysis circuit play an additional role.
What medications decrease GFR? ›Non-steroidal anti-inflammatory drugs (NSAIDs)
All the NSAIDs inhibit prostaglandin synthesis, leading to unopposed, intrarenal vasoconstriction. This decreases the glomerular filtration rate.
Angiotensin converting enzyme inhibitors such as captopril and enalapril have produced increased renal blood flow and well-maintained glomerular filtration in patients with essential hypertension.
What is the effect of prostaglandin on afferent arteriole? ›Our findings indicate that PGE2 exerts a selective effect on the afferent arteriole, eliciting both vasodilation and vasoconstriction of this vessel.
Do ACE inhibitors affect afferent arteriole? ›Unlike the direct-acting smooth muscle vasodilators or adrenergic inhibitors, ACE inhibitors dilate the efferent as well as the afferent glomerular arterioles and thereby reduce glomerular hydrostatic pressure and renal filtration fraction, even though renal blood flow and glomerular filtration rate are preserved.
Does ibuprofen constrict afferent arteriole? ›Because ibuprofen inhibits the formation of prostaglandin, our afferent arteriole's begin to constrict without a signal to dilate due to the absence of the hormone. As a result, there is a decrease of blood flow in the kidney and therefore filtration is also reduced.
What is the mechanism of NSAID nephrotoxicity? ›
The nephrotoxic effects of NSAIDs arise mainly from two pathological mechanisms: (1) acute tubulo-interstitial nephritis (ATIN) following immune reaction and (2) prerenal failure because of reduced renal plasma flow. Histological examinations are required to confirm the pathomechanism of AKI after NSAID exposure.
Can ibuprofen cause renal tubular acidosis? ›Ibuprofen-induced distal RTA is related to the drug's inhibitory effect on carbonic anhydrase II, resulting in impaired urinary acidification, urinary bicarbonate retention, and compensatory reduction in chloride excretion so as to maintain tubular electroneutrality. Ng J.L. Morgan D.J.R.
Why is ibuprofen bad for CKD? ›Also, even if your kidney function is good, long–term use with high doses of these pain drugs may harm the kidneys. Kidney damage happens because high doses of the drugs have a harmful effect on kidney tissue and structures. These drugs can also reduce the blood flow to the kidney.
Do ACE inhibitors worsen renal function? ›During ACEI initiation, renal dysfunction can occur due to a drop in renal perfusion pressure and subsequent decrease in glomerular filtration. This is attributed to the drug's preferential vasodilation of the renal efferent arteriole, which impairs the kidney's ability to compensate for low perfusion states.
At what GFR should ACE inhibitors be stopped? ›Accordingly, in patients with CKD stage 5 (eGFR <15 mL/min per 1.73 m2), the guidelines recommend reducing the dose or discontinuing ACE inhibitors or ARBs in the setting of either symptomatic hypotension or uncontrolled hyperkalemia [1,2,3].
Can lisinopril worsen kidney function? ›The short answer is that lisinopril doesn't usually harm your kidneys. Rather, it's been shown to have several benefits for the kidneys. But if you have certain risk factors, it could affect how well your kidneys work.
What are prostaglandins renal actions? ›Renal prostaglandins act primarily as local hormones, having their effects at, or near to, sites of synthesis. PGE2 is a major determinant of renal vascular reactivity; it opposes the vasoconstrictor and natriuretic actions of pressor hormones and brakes the release of noradrenaline from adrenergic nerves.
What effect does prostaglandin have on the arteriole? ›Certain conditions that promote renal vasoconstriction and renal hypoperfusion require prostaglandins to vasodilate the afferent arteriole and blunt vasoconstriction to maintain a normal GFR (left).
What is prostaglandin in kidney disease? ›Studies have shown that PGs exert multiple physiological functions in the kidney, such as maintaining glomerular filtration, modulating water and sodium excretion. Moreover, PGs are also involved in the pathology of various renal diseases including CKD and AKI.
What do prostaglandins do on afferent arteriole? ›Our findings indicate that PGE2 exerts a selective effect on the afferent arteriole, eliciting both vasodilation and vasoconstriction of this vessel. The vasodilation appears to be mediated by the EP4 receptor coupled to a cAMP-dependent mechanism.
How do prostaglandins affect blood pressure? ›
One of the most striking actions of prostaglandins of the E and A series is their capacity to dilate peripheral blood vessels and thereby to lower arterial pressure.
How do prostaglandins increase blood pressure? ›Abstract. In normotensive and hypertensive humans, prostaglandins, particularly PGE2 and PGI2, affect blood pressure through control of vascular resistance, salt excretion, cardiac output, and renin secretion.
Do all NSAIDs affect the kidneys? ›NSAIDs may increase your fluid retention and can lead to decreased blood flow to kidneys. This is because NSAIDs block prostaglandins, which are the natural chemicals that dilate blood vessels and allow oxygen to reach the kidneys to keep them alive and healthy.
How do prostaglandins affect blood flow? ›Prostaglandins can: Activate or inhibit (prevent) platelet buildup for blood clot formation. Cause vasodilation (widening of blood vessels) or vasoconstriction (narrowing of blood vessels). Cause bronchoconstriction (the narrowing of air passageways) or bronchodilation (widening of air passageways).
Do prostaglandins cause vasodilation or vasoconstriction? ›Prostaglandins induce vasodilatation of the microvasculature during muscle contraction and induce vasodilatation independent of adenosine.
Do prostaglandins dilate afferent arteriole? ›COX-derived prostaglandins play a critical role in modulating renal blood flow and glomerular filtration (Hao, 2008). PGI2 and PGE2 are primarily vasodilatory, preferentially vasodilating the afferent arteriole (Kim, 2008; Edwards, 1985).
What are the adverse side effects of prostaglandin? ›[10] Vaginally administered prostaglandins may cause symptoms such as nausea, vomiting, flushing, fever, back pain, diarrhea, and abdominal pain. [11] When using alprostadil for erectile dysfunction, serious side effects such as priapism can occur as well.
Do prostaglandins constrict the efferent arteriole? ›Although these two hormonal systems exert opposite effects on systemic and renal blood flow and sodium and water excretion, both act to preserve glomerular filtration rate: prostaglandins by a vasodilator action exerted primarily on the afferent arteriole and angiotensin II by a vasoconstrictor effect on the efferent ...
What are the factors affecting renal blood flow? ›Renal blood flow is regulated by the autonomic nervous system, hormones, and local autoregulation mechanisms. The autonomic nervous system, primarily the sympathetic nervous system, can increase or decrease renal blood flow by constricting or dilating renal arterioles.
Do prostaglandins increase blood vessel permeability? ›Using 85Sr-microspheres to measure blood flow a correlation was found between the degree of hyperemia produced by prostaglandins and the degree to which they augmented enhanced vascular permeability due to histamine, serotonin or bradykinin.