Acetylcholine-induced vasodilatation in the human hypertensive kidney

Wierema, Thomas K.A.; Houben, A. J. H. M.; Leeuw, Peter W. de

doi:10.1097/00004872-199715120-00067

Cited by 9 publications

(10 citation statements)

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“…[50][51][52][53] In addition, the activation of muscarinic receptors by acetylcholine induces vasodilatation and increases renal blood flow. [54] Therefore, muscarinic acetylcholine receptors seem to perform an important role in triggering the renal effects of MG, as the pretreatment with atropine completely prevented its diuretic and saluretic effects. On the other hand, while indomethacin was entirely inert to the effects of MG, L-NAME was able to amplify its diuretic effect.…”

Section: Discussionmentioning

confidence: 99%

“…The major vasodilatory agents studied include the prostanoids produced by cyclooxygenase enzyme and nitric oxide released by the different isoforms of the enzyme nitric oxide synthase . In addition, the activation of muscarinic receptors by acetylcholine induces vasodilatation and increases renal blood flow . Therefore, muscarinic acetylcholine receptors seem to perform an important role in triggering the renal effects of MG, as the pretreatment with atropine completely prevented its diuretic and saluretic effects.…”

Section: Discussionmentioning

confidence: 99%

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Chemical composition and diuretic, natriuretic and kaliuretic effects of extracts ofMimosa bimucronata(DC.) Kuntze leaves and its majority constituent methyl gallate in rats

Schlickmann

Souza

Boeing

et al. 2017

Journal of Pharmacy and Pharmacology

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chemical composition and diuretic, natriuretic and kaliuretic effects of extracts ofMimosa bimucronata(DC.) Kuntze leaves and its majority constituent methyl gallate in rats

Schlickmann

Souza

Boeing

et al. 2017

Journal of Pharmacy and Pharmacology

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“…However, in earlier studies we showed that both acetylcholine and adenosine induce renal vasodilatation, and that this was adequately detected with our method. 19,20 So, if there was any (net) effect of BNP, it must have been very small. Another limitation of the present study is that for ethical reasons, we could not study healthy subjects.…”

Section: Limitationsmentioning

confidence: 99%

Does Brain Natriuretic Peptide Have a Direct Renal Effect in Human Hypertensives?

Zander

Houben²,

Wierema³

et al. 2003

Hypertension

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Abstract-Systemic infusion of brain natriuretic peptide (BNP) stimulates natriuresis and diuresis but has variable effects on the renal vasculature. In this study, we investigated whether BNP has any direct effects on the kidney in hypertensive patients. Three stepwise increasing doses of BNP (60, 120, and 180 pmol/min) or placebo were infused into the renal artery of 26 hypertensive patients. Renal blood flow was determined with the 133 Xenon washout technique. Before and after infusion of BNP, arterial and venous blood samples were taken for cGMP, renin, and creatinine concentration. Intra-arterial blood pressure and heart rate were monitored continuously. Intrarenal BNP infusion did not induce significant changes in renal blood flow despite increases in circulating levels of cGMP. The latter, however, was not associated with changes in the cGMP gradient across the kidney. In addition, we did not find any BNP-related changes in the secretion of active renin and in creatinine extraction. At the highest dose, heart rate increased after BNP infusion without a change in mean intra-arterial blood pressure. In conclusion, this study suggests that at least in hypertensive subjects, BNP has no direct intrarenal hemodynamic effects and that the rise in circulating cGMP without changes in net renal extraction of this second messenger is related to a primary extrarenal target of BNP. Key Words: natriuretic peptides Ⅲ vasodilation Ⅲ hypertension, renal Ⅲ human Ⅲ kidney Ⅲ hemodynamics Ⅲ vasoconstriction Ⅲ hormones S ystemic infusion of brain natriuretic peptide (BNP) stimulates natriuresis and diuresis 1-6 and inhibits plasma renin activity [1][2][3]7,8 but has variable effects on the renal vasculature. Although most but not all studies in healthy humans reported that BNP infusion increases glomerular filtration rate, 1,5-7 renal plasma flow has been found to decrease, 1,7 to increase, 5 or to remain unchanged. 3,8 Variations in the renovascular effects of BNP could be related to differences in BNP levels reached during the experiments, but it is equally possible that the renal changes are, in part, secondary to systemic effects. Indeed, BNP not only acts on the kidney but also affects blood pressure, heart rate, cardiac output, and systemic vascular resistance. 2,3,5,6,8,9 In those studies in which changes in renal plasma flow are reported, it is important to keep in mind that such alterations may simply be due to concurrent changes in cardiac output. If, for instance, renal fraction (that is, the proportion of cardiac output perfusing the kidneys) remains unaltered during systemic BNP infusion, it is unlikely that the peptide has exerted a direct effect on the renal vasculature. If, on the other hand, renal fraction increases, relative renal vasodilation must have occurred. In most studies, this has not been taken into account.Local administration of BNP in a regional vascular bed in amounts that will not have systemic effects allows for assessing whether BNP has any direct effects on certain parts of the circulation. Wi...

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Section: Choice Of Vasoactive Substancementioning

confidence: 99%

“…Among these, papaverine dilates the renal microcirculation and is more likely to achieve a substantial decrease in RVR and RFR than conduit vessel dilators. However, acetylcholine, 3,5,6,12,13,[47][48][49] the prototypical endothelium-dependent vasodilator of the microcirculation, appears to be associated with greater RFR attended by a smaller and more transient decrease in MAP.Indeed, using EBCT, we have observed that systemic administration of acetylcholine effectively increased RBF (Figure, part a) accompanied by only a transient decrease in MAP, whereas the dose of sodium nitroprusside required to increase RBF was accompanied by a small but sustained decrease in MAP. 37,40 Intrarenal bolus injections of acetylcholine also dose dependently increased RBF (measured using intravascular Doppler) more effectively than papaverine, in association with smaller decrements in MAP (Figure, part b), suggesting that acetylcholine may be a suitable challenge for RFR.…”

mentioning

confidence: 99%

Functional Assessment of the Circulation of the Single Kidney

Lerman

Rodriguez-Porcel²

2001

Hypertension

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Abstract-Functional alterations in the renal circulation that can contribute to abnormal renal perfusion have been demonstrated in various models of renal injury. To detect impairments in renal vascular function, renal flow reserve can be determined by repeated measurements of renal blood flow (RBF) during pharmacological challenge with short-acting vasodilators that should increase RBF in kidneys that are not severely damaged structurally. Among the invasive techniques for such measurements, the most readily available is probably the intravascular Doppler, which can be employed during renal angiography for rapid evaluation of changes in RBF during intrarenal injections of vasoactive substances. High-resolution tomographic imaging techniques, like electron-beam x-ray computed tomography, further offer the potential for noninvasive measurements of renal parenchymal perfusion and function, in association with either intrarenal or systemic injections of vasoactive substances. Acetylcholine is a potent short-acting renal vasodilator that can be useful to assess the response of the renal microcirculation, define renal flow reserve, and examine the endothelium-dependent responses of RBF. Such assessments of the function of the renal circulation can assist in evaluation of patients with systemic or renal disease for early detection and monitoring of renovascular injury. Key Words: renal circulation Ⅲ renal blood flow Ⅲ computed tomography Ⅲ acetylcholine U nder normal conditions, basal renal vascular tone is well regulated by many vasoactive systems that keep renal blood flow (RBF) in equilibrium, 1 including the endothelium-derived relaxing factor NO, prostaglandins, and the reninangiotensin system. 2 Therefore, at an early stage of renal disease, RBF may be normal, and impaired renal vascular tone may become evident only as an attenuated response during stimulus with vasoactive substances or physiological challenges. The mechanisms of the attenuated response have been postulated to include decreased release of vasodilators (eg, NO, prostaglandins) and co-existing vasoconstrictors (eg, thromboxane, angiotensin II), which may be released or rendered unopposed during challenge. The altered functional response may precede structural renal damage and can serve as a marker for abnormal handling of daily challenges by the kidney. Such impairment has been demonstrated in various models of renal injury, like hypertension, hypercholesterolemia, renal artery stenosis, ischemia and reperfusion, acute renal failure, diabetes mellitus, and aging. Hence, utilization of vasodilators to examine renal flow reserve (RFR) can serve to disclose subtle functional vascular alterations 3 and may allow early detection and monitoring of renovascular injury. For example, residual responsiveness of the intrarenal circulation to challenge may also reflect renal viability and may conceivably predict success of subsequent therapy (eg, revascularization).Evaluation of the reactivity of the single-kidney circulation entails rapid and successive meas...

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Acetylcholine-induced vasodilatation in the human hypertensive kidney

Abstract: Administration of ACh to the human hypertensive kidney induces a dose-dependent increase in renal blood flow. This effect is, at least partially, mediated by muscarinic receptors.

Cited by 9 publications

References 10 publications

Chemical composition and diuretic, natriuretic and kaliuretic effects of extracts ofMimosa bimucronata(DC.) Kuntze leaves and its majority constituent methyl gallate in rats

Chemical composition and diuretic, natriuretic and kaliuretic effects of extracts ofMimosa bimucronata(DC.) Kuntze leaves and its majority constituent methyl gallate in rats

Does Brain Natriuretic Peptide Have a Direct Renal Effect in Human Hypertensives?

Functional Assessment of the Circulation of the Single Kidney

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