Contribution of the renin‐angiotensin system to short‐term blood pressure variability during blockade of nitric oxide synthesis in the rat

O, Gouédard; Blanc, Jocelyne; Gaudet, E; Ponchon, Pascal; Elghozi, Jean‐Luc

doi:10.1111/j.1476-5381.1996.tb16008.x

Cited by 40 publications

(31 citation statements)

References 43 publications

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“…Administration of PE may be analogous to baroreflex denervation in that baroreflex-mediated changes in peripheral vascular resistance may be largely attenuated because of the chronic stimulation of ␣ 1 -adrenergic receptors. Other factors have also been reported to modulate VLF BP oscillations, including the RAAS and nitric oxide (15,22). To this extent, our data are also in agreement with these previous studies, as evidenced by the ANG II-induced increase in VLF BP power, although to a significantly lesser extent compared with PE-infused rats.…”

Section: Discussionsupporting

confidence: 82%

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: Discussionsupporting

confidence: 82%

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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“…Consistent with our previous report (7), BPV was lower in mice lacking ANG AT1a receptors. Pharmacological intervention with angiotensin receptor blockers also decreased BPV (22,25). Treatment with STZ produced a prominent reduction in BPV in controls with no effect in AT1aKO.…”

Section: Discussionmentioning

confidence: 92%

Deficiency in angiotensin AT1a receptors prevents diabetes-induced hypertension

Wichi

Farah²,

Chen³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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The renin-angiotensin system has been implicated in the etiology of the cardiovascular complications of diabetes. Our studies extend these findings to show a specific role for angiotensin AT1a receptors in mediating diabetes-induced hypertension. Male angiotensin AT1a knockout (AT1aKO) and wild-type (AT1aWT) mice with arterial telemetric catheters were injected with streptozotocin (STZ; 150 mg/kg ip). The STZ dose was selected on the basis of a dose-response experiment in C57/BL mice. Blood glucose, water intake, body weight, blood pressure (BP), and heart rate (HR) were measured over a 2-wk period. Estimates of BP and HR variance (BPV and HRV) and their low-and high-frequency domains were also determined. STZ induced similar levels of hyperglycemia and polydypsia in the groups. Mean arterial pressure (MAP) was increased from 100 Ϯ 6 to 124 Ϯ 6 mmHg in diabetic AT1aWT. MAP was unchanged in AT1aKO (80 Ϯ 4 vs. 85 Ϯ 5 mmHg, basal vs. STZ). Treatment with an ACE inhibitor, captopril, produced a greater reduction in MAP (Ϫ18%) in diabetic AT1aWT than in AT1aKO (Ϫ3.4%). BPV was lower in AT1aKO (19 Ϯ 0.5 vs. 9 Ϯ 2 mmHg 2 , AT1aWT vs. AT1aKO). Diabetes reduced BPV but only in AT1aWT (19 Ϯ 0.5 vs. 8 Ϯ 1 mmHg 2 , basal vs. STZ). There were no changes in HR in either group. In AT1aKO, STZ increased HRV and its high-frequency domain with no changes seen in AT1aWT. Results document that ANG AT1a receptors are critical in diabetes-induced hypertension and in cardiac autonomic responses. cardiovascular; heart rate; blood pressure; renin-angiotensin system; mice; autonomic function; streptozotocin; diabetes DIABETES MELLITUS IS A RISK factor for the development of cardiovascular disease, such as hypertension, atherosclerosis, and congestive heart failure. Mortality rates are greater in diabetic compared with nondiabetic persons, and cardiovascular disease in diabetic patients further increases the risk. The hallmark symptom for diabetes is hyperglycemia, resulting from ␤-cell damage (Type 1) or insulin resistance (Type 2). Hyperglycemia is thought to be a major determinant in the development of longterm complications of diabetes, and treatment is focused on strict glycemic control (1, 23). However, there are interactions with the renin-angiotensin system (RAS), which contribute to diabetesinduced organ damage (8,23,43,53).The RAS plays an important role in the regulation of blood pressure and volume, mainly via the actions of ANG II. Most of the cardiovascular effects of ANG II are mediated by AT1 receptors, which are present in vasculature, brain, heart, and other tissues. AT1 receptors exist as two subtypes, AT1a and AT1b, in mice and rats (33). Studies of the functional role of AT1a receptors have relied on gene deletion (30) or gene silencing (5) methods, because it is not possible to pharmacologically distinguish AT1 receptors. ANG AT1a-deficient mice show low blood pressure, altered renal and autonomic function, and increased sodium sensitivity (6,30,45,46,49,50).Diabetes is associated with activation of the RAS in both h...

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“…However, very low-frequency (VLF) blood pressure fluctuations (0.02-0.2 Hz in rats) at frequencies below the frequency of Mayer waves are less well understood. A variety of factors, including catecholamines (45), the renin-angiotensin system (7,18,43,44), heat stress (51), and hypovolemia (42), have been associated with VLF blood pressure variability. In addition, studies on dynamic autoregulation of local blood flow in rats demonstrated that myogenic vascular function is most effective at frequencies Ͻ0.2 Hz in the renal circulation (1, 9, 30, 53), Ͻ0.13 Hz in the mesenteric vascular bed (1), and Ͻ0.1 Hz in the cerebral circulation (27).…”

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confidence: 99%

Very low-frequency blood pressure variability depends on voltage-gated L-type Ca²⁺channels in conscious rats

Langager

Hammerberg²,

Rotella³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Langager AM, Hammerberg BE, Rotella DL, Stauss HM. Very low-frequency blood pressure variability depends on voltage-gated L-type Ca 2ϩ channels in conscious rats. Am J Physiol Heart Circ Physiol 292: H1321-H1327, 2007. First published October 20, 2006; doi:10.1152/ajpheart.00874.2006.-The mechanisms generating highfrequency (HF) and low-frequency (LF) blood pressure variability (BPV) are reasonably well understood. However, little is known about the origin of very low-frequency (VLF) BPV. We tested the hypothesis that VLF BPV is generated by L-type Ca 2ϩ channel-dependent mechanisms. In conscious rats, arterial blood pressure was recorded during control conditions (n ϭ 8) and ganglionic blockade (n ϭ 7) while increasing doses (0.01-5.0 mg ⅐ 100 l Ϫ1 ⅐ h Ϫ1 ) of the L-type Ca 2ϩ channel blocker nifedipine were infused intravenously. VLF (0.02-0.2 Hz), LF (0.2-0.6 Hz), and HF (0.6 -3.0 Hz) BPV were assessed by spectral analysis of systolic blood pressure. During control conditions, nifedipine caused dose-dependent declines in VLF and LF BPV, whereas HF BPV was not affected. At the highest dose of nifedipine, VLF BPV was reduced by 86% compared with baseline, indicating that VLF BPV is largely mediated by L-type Ca 2ϩ channeldependent mechanisms. VLF BPV appeared to be relatively more dependent on L-type Ca 2ϩ channels than LF BPV because lower doses of nifedipine were required to significantly reduce VLF BPV than to reduce LF BPV. Ganglionic blockade markedly reduced VLF and LF BPV and abolished the nifedipine-induced dose-dependent declines in VLF and LF BPV, suggesting that VLF and LF BPV require sympathetic activity to be evident. In conclusion, VLF BPV is largely mediated by L-type Ca 2ϩ channel-dependent mechanisms. We speculate that VLF BPV is generated by myogenic vascular responses to spontaneously occurring perturbations of blood pressure. Other factors, such as sympathetic nervous system activity, may elicit a permissive effect on VLF BPV by increasing vascular myogenic responsiveness. power spectral analysis; myogenic vascular function; nifedipine; autonomic nervous system; ganglionic blockade BLOOD PRESSURE VARIABILITY has received considerable attention during the last decades, not only because enhanced blood pressure variability has been identified as an independent cardiovascular risk factor (33, 35) but also because the patterns of blood pressure variability may provide important insights into cardiovascular regulation (2, 23, 31). Highfrequency (HF) blood pressure variability linked to respiration has been suggested to involve fluctuations in cardiac output of purely mechanical origin (23), secondary to respiratory sinus arrhythmia (2). Low-frequency (LF) blood pressure fluctuations (0.2-0.6 Hz in rats), the so-called Mayer waves (36), have been associated mostly with sympathetic modulation of vascular tone (22, 50, 52). However, very low-frequency (VLF) blood pressure fluctuations (0.02-0.2 Hz in rats) at frequencies below the frequency of Mayer waves are less well understood. A variety of facto...

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Contribution of the renin‐angiotensin system to short‐term blood pressure variability during blockade of nitric oxide synthesis in the rat

Cited by 40 publications

References 43 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

Deficiency in angiotensin AT1a receptors prevents diabetes-induced hypertension

Very low-frequency blood pressure variability depends on voltage-gated L-type Ca²⁺channels in conscious rats

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Contribution of the renin‐angiotensin system to short‐term blood pressure variability during blockade of nitric oxide synthesis in the rat

Cited by 40 publications

References 43 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

Deficiency in angiotensin AT1a receptors prevents diabetes-induced hypertension

Very low-frequency blood pressure variability depends on voltage-gated L-type Ca2+channels in conscious rats

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Very low-frequency blood pressure variability depends on voltage-gated L-type Ca²⁺channels in conscious rats