Role of angiotensin II in dynamic renal blood flow autoregulation of the conscious dog

Just, Armin; Ehmke, Heimo; Wittmann, U.; Kirchheim, H. R.

doi:10.1113/jphysiol.2001.012593

Cited by 32 publications

(48 citation statements)

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“…These changes were paralleled by significant changes in phase peak, coherence, and slope-of-gain reduction. Just et al (47) similarly reported a significant potentiation of the myogenic resonance peak during ANG II infusion in conscious dogs. These effects of ANG II on the myogenic mechanism are consistent with the observed pattern of the BP-RBF relationships that we observed.…”

Section: Discussionmentioning

confidence: 82%

“…Just et al (47) did not observe a significant effect of ANG II on the operating frequency of the myogenic mechanism in conscious, resting dogs. While the reasons for such differences between studies are not readily apparent, some potential explanations include acute vs. chronic ANG II administration, differences in the level of BP achieved during ANG II, as well as species differences.…”

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confidence: 99%

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Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Polichnowski

Griffin

Long

et al. 2013

American Journal of Physiology-Renal Physiology

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Polichnowski AJ, Griffin KA, Long J, Williamson GA, Bidani AK. Blood pressure-renal blood flow relationships in conscious angiotensin II-and phenylephrine-infused rats. Am J Physiol Renal Physiol 305: F1074 -F1084, 2013. First published July 3, 2013 doi:10.1152/ajprenal.00111.2013.-Chronic ANG II infusion in rodents is widely used as an experimental model of hypertension, yet very limited data are available describing the resulting blood pressurerenal blood flow (BP-RBF) relationships in conscious rats. Accordingly, male Sprague-Dawley rats (n ϭ 19) were instrumented for chronic measurements of BP (radiotelemetry) and RBF (Transonic Systems, Ithaca, NY). One week later, two or three separate 2-h recordings of BP and RBF were obtained in conscious rats at 24-h intervals, in addition to separate 24-h BP recordings. Rats were then administered either ANG II (n ϭ 11, 125 ng·kg Ϫ1 ·min Ϫ1 ) or phenylephrine (PE; n ϭ 8, 50 mg·kg Ϫ1 ·day Ϫ1 ) as a control, ANG IIindependent, pressor agent. Three days later the BP-RBF and 24-h BP recordings were repeated over several days. Despite similar increases in BP, PE led to significantly greater BP lability at the heart beat and very low frequency bandwidths. Conversely, ANG II, but not PE, caused significant renal vasoconstriction (a 62% increase in renal vascular resistance and a 21% decrease in RBF) and increased variability in BP-RBF relationships. Transfer function analysis of BP (input) and RBF (output) were consistent with a significant potentiation of the renal myogenic mechanism during ANG II administration, likely contributing, in part, to the exaggerated reductions in RBF during periods of BP elevations. We conclude that relatively equipressor doses of ANG II and PE lead to greatly different ambient BP profiles and effects on the renal vasculature when assessed in conscious rats. These data may have important implications regarding the pathogenesis of hypertension-induced injury in these models of hypertension.hypertension; hemodynamics; blood pressure variability INCREASED ACTIVITY OF THE renin-angiotensin-aldosterone system (RAAS) (40,56,73) is postulated to be a major contributor to chronic kidney disease progression through both blood pressure (BP)-dependent and -independent mechanisms (7,28,39,73). Accordingly, chronic ANG II infusion is extensively used to investigate mechanisms that mediate renal damage in hypertensive states characterized by enhanced RAAS activation (3,20,42,65,71). Renal parenchymal injury with significant tubulointerstitial fibrosis and a propensity to develop salt-sensitive hypertension has been observed after ANG II infusions (44, 57). Both barotrauma and renal vasoconstrictionmediated tissue ischemia have been postulated to initiate the pathogenic cascades that lead to renal injury after chronic ANG II infusions. However, despite its wide use, there is a paucity of experimental data describing the BP-renal blood flow (RBF) relationships in conscious ANG II-infused animals, and the relative contribution of these two initiating mechanisms ...

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Section: Discussionmentioning

confidence: 82%

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confidence: 99%

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Polichnowski

Griffin

Long

et al. 2013

American Journal of Physiology-Renal Physiology

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“…The juxtaglomerular apparatus also participates in regulating the synthesis and release of renin, the rate-limiting enzyme for the production of AngII. This peptide is known to play an important role in resetting myogenic responses and TGF (20,24,25). During salt restriction, increased AngII enhances the sensitivity of the myogenic response (25) and shifts the TGF curve to the left, thereby preventing further loss of NaCl.…”

Section: Discussionmentioning

confidence: 99%

“…This peptide is known to play an important role in resetting myogenic responses and TGF (20,24,25). During salt restriction, increased AngII enhances the sensitivity of the myogenic response (25) and shifts the TGF curve to the left, thereby preventing further loss of NaCl. During salt loading, the sensitivity of the myogenic response is diminished, and the TGF curve shifts to the right, with a decrease in AngII production.…”

Section: Discussionmentioning

confidence: 99%

Alterations in Renal Endothelial Nitric Oxide Synthase Expression by Salt Diet in Angiotensin Type-1a Receptor Gene Knockout Mice

Satô

Kihara²,

Hashimoto³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. The effects of altered dietary salt intake and/or hydralazine-induced hypotension on renal endothelial nitric oxide synthase (eNOS) expression were determined in angiotensin type-1a receptor gene knockout (At1aϪ/Ϫ) and wild-type (At1aϩ/ϩ) mice. In At1aϪ/Ϫ mice, the levels of renal cortical eNOS mRNA and protein were 5 times and 3.5 times higher, respectively, in the high-salt (4% NaCl) group than in the low-salt group (0.3% NaCl). Systemic BP of the high-salt group (105 Ϯ 4.4 mmHg) was significantly higher than that of the low-salt group (77.0 Ϯ 4.7 mmHg). When hydralazine was administered to the mutant mice fed a high-salt diet, BP was reduced to 72.5 Ϯ 1.3 mmHg, with decreases in the levels of renal eNOS mRNA and protein expression to about half of those found in nontreated group. Consistent with the results for eNOS mRNA and protein expression, nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase activity and eNOS immunoreactivity localized in the endothelium of the renal vasculature changed parallel with the amount of salt intake. In contrast to mutant mice, At1aϩ/ϩ mice did not show any changes in renal eNOS expression during the manipulation of salt intake and/or hydralazine-induced hypotension. These results suggest that At1a receptor-mediated inputs play critical roles in maintaining renal vascular eNOS expression and activity during changes in salt-water balance and systemic BP.The endothelial nitric oxide synthase (eNOS) is distributed throughout the renal vasculature, from the renal arterial branches to the glomerular capillaries. NO synthesized by eNOS in response to renal perfusion pressure and the tubuloglomerular feedback system is thought to be an important modulator of vascular tone. Renal perfusion pressure has been shown to increase urinary NO 2 /NO 3 excretion as well as output current from an electrode inserted into the renal cortex (1).eNOS is a constitutively expressed enzyme responsible for the generation of basal NO release from endothelial cells. The major stimuli of enzyme activity include shear stress and/or pressure stretch. In the kidney, however, the regulation of eNOS activity under various physiologic conditions is not well understood. Previous experiments testing the effects of altered salt intake or BP on renal eNOS activity have yielded inconsistent results (2-8).While there is little information on the endogenous factors that regulate eNOS expression within the kidney, angiotensin II

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“…15 Ang II levels also do not seem to modulate the relative contributions of MR and TGF. 27,38 We and others have shown that NO exerts a strong attenuating influence on the MR in the renal but not nonrenal circulations. 27,28 Importantly, this NO influence depends on functional TGF, 27,28 suggesting neuronal NOS in macula densa cells as the source.…”

Section: Discussionmentioning

confidence: 99%

Connexin 40 Mediates the Tubuloglomerular Feedback Contribution to Renal Blood Flow Autoregulation

Just

Kurtz

Wit

et al. 2009

Journal of the American Society of Nephrology

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Connexins are important in vascular development and function. Connexin 40 (Cx40), which plays a predominant role in the formation of gap junctions in the vasculature, participates in the autoregulation of renal blood flow (RBF), but the underlying mechanisms are unknown. Here, Cx40-deficient mice (Cx40-ko) had impaired steady-state autoregulation to a sudden step increase in renal perfusion pressure. Analysis of the mechanisms underlying this derangement suggested that a marked reduction in tubuloglomerular feedback (TGF) in Cx40-ko mice was responsible. In transgenic mice with Cx40 replaced by Cx45, steady-state autoregulation and TGF were weaker than those in wild-type mice but stronger than those in Cx40-ko mice. N-Nitro-L-arginine-methyl-ester (L-NAME) augmented the myogenic response similarly in all genotypes, leaving autoregulation impaired in transgenic animals. The responses of renovascular resistance and arterial pressure to norepinephrine and acetylcholine were similar in all groups before or after L-NAME inhibition. Systemic and renal vasoconstrictor responses to L-NAME were also similar in all genotypes. We conclude that Cx40 contributes to RBF autoregulation by transducing TGF-mediated signals to the afferent arteriole, a function that is independent of nitric oxide (NO). However, Cx40 is not required for the modulation of the renal myogenic response by NO, norepinephrine-induced renal vasoconstriction, and acetylcholine-or NO-induced vasodilation.

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Role of angiotensin II in dynamic renal blood flow autoregulation of the conscious dog

Cited by 32 publications

References 48 publications

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Blood pressure-renal blood flow relationships in conscious angiotensin II- and phenylephrine-infused rats

Alterations in Renal Endothelial Nitric Oxide Synthase Expression by Salt Diet in Angiotensin Type-1a Receptor Gene Knockout Mice

Connexin 40 Mediates the Tubuloglomerular Feedback Contribution to Renal Blood Flow Autoregulation

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