Renal vascular resistance and reactivity in the spontaneously hypertensive rat

1979 ◽  
Vol 237 (2) ◽  
pp. F128-F132 ◽  
Author(s):  
G. D. Fink ◽  
M. J. Brody
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Renal Vascular Resistance ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Spontaneously Hypertensive ◽  
Wide Range ◽  
Renal Nerve Stimulation ◽  
Renal Vascular

Renal vascular resistance is elevated in spontaneously hypertensive rats (SHR) when compared to normotensive control Wistar-Kyoto rats (WKY). The present study examined possible determinants of this raised vascular resistance in in situ autoperfused kidneys of pentobarbital-anesthetized, 12- to 16-wk-old SHR and WKY. Over a wide range of arterial pressures (30––100 mmHg) renal blood flow was consistently higher in WKY than in SHR. This relative flow difference was unchanged by acute renal denervation, with renal vascular resistance decreasing approximately 20% in both strains. Changes in renal vascular resistance to renal nerve stimulation and the administration of intra-arterial vasoactive hormones also were assessed. Vascular responses to renal nerve stimulation, tyramine, angiotensin II, and acetylcholine were similar in kidneys of the two strains, but reactivity to norepinephrine was significantly less in kidneys of SHR. It was concluded that elevated renal vascular resistance in the SHR does not result from an excessive neurogenic influence on the renal vasculature or from vascular hyperreactivity to norepinephrine or angiotensin II.

Attenuation by prostaglandins of adrenergically induced renal vasoconstriction in anesthetized rats

1984 ◽  
Vol 246 (2) ◽  
pp. R228-R235
Author(s):  
K. Inokuchi ◽  
K. U. Malik
Keyword(s):  
Arachidonic Acid ◽  
Renal Artery ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Renal Vascular Resistance ◽  
Cyclooxygenase Inhibitor ◽  
Renal Nerve ◽  
Vasoconstrictor Response ◽  
Renal Nerve Stimulation ◽  
Renal Vascular

We have investigated the role of prostaglandins (PG) in the modulation of adrenergic neuroeffector events by examining the effect of PGI2 and PGE2 and their precursor, arachidonic acid, on the decrease in renal blood flow elicited by renal nerve stimulation or by injected norepinephrine in pentobarbital-anesthetized rats, with or without pretreatment with the cyclooxygenase inhibitor, sodium meclofenamate. Administration of PGI2 or PGE2 (0.4 micrograms X kg-1 X min-1) or arachidonic acid (5 micrograms X kg-1 X min-1) into the renal artery reduced vascular resistance and inhibited the vasoconstrictor response elicited by renal nerve stimulation or by injected norepinephrine. In contrast, administration of sodium meclofenamate (10 mg/kg iv + 30 micrograms X kg-1 X min-1) into the renal artery increased renal vascular resistance and enhanced the renal vasoconstrictor response to both adrenergic stimuli. In animals pretreated with the cyclooxygenase inhibitor, the ability of arachidonic acid, but not that of either PGE2 or PGI2, to reduce renal vascular resistance and the vasoconstrictor response to either nerve stimulation or injected norepinephrine was abolished. These data indicate that one or more prostaglandins, probably PGE2 or PGI2, formed in the kidney reduce renal vascular tone by their direct action on the vascular smooth muscle and by attenuating the influence of adrenergic stimuli on renal vasculature.

Inhibition by bradykinin of renal adrenergic effects in anesthetized rats

1984 ◽  
Vol 246 (4) ◽  
pp. F387-F394
Author(s):  
K. Inokuchi ◽  
K. U. Malik
Keyword(s):  
Arachidonic Acid ◽  
Renal Artery ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Rat Kidney ◽  
Renal Vascular Resistance ◽  
Cyclooxygenase Inhibitors ◽  
Renal Nerve ◽  
Anesthetized Rats ◽  
Renal Vascular

We studied the contribution of prostaglandins to the actions of bradykinin at the renal vascular adrenergic neuroeffector junction by examining the effect of the peptide on the decrease in renal blood flow elicited by renal nerve stimulation and injected norepinephrine in pentobarbital-anesthetized rats with or without pretreatment with the cyclooxygenase inhibitors sodium meclofenamate or indomethacin. Infusion of bradykinin, 10 ng X kg-1 X min-1, into the renal artery reduced both the basal and the rise in renal vascular resistance produced by nerve stimulation or norepinephrine. The prostaglandin precursor arachidonic acid, 5 micrograms X kg-1 X min-1, infused into the renal artery, also reduced renal vascular resistance and the vasoconstrictor response elicited by either adrenergic stimulus. In animals pretreated with either sodium meclofenamate or indomethacin, the effect of arachidonic acid, but not that of bradykinin, to produce renal vasodilation and to attenuate adrenergically induced renal vasoconstriction was abolished. These data suggest that bradykinin produces renal vasodilation and inhibits the renal vasoconstrictor effect of adrenergic stimuli in the rat kidney in vivo by a mechanism unrelated to prostaglandin synthesis.

Losartan corrects abnormal frequency response of renal vasculature in congestive heart failure

2003 ◽  
Vol 285 (5) ◽  
pp. H1857-H1863 ◽  
Author(s):  
Gerald F. DiBona ◽  
Linda L. Sawin
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Angiotensin Ii ◽  
Frequency Response ◽  
Nerve Stimulation ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Pass Filter ◽  
Vasoconstrictor Response ◽  
Renal Nerve Stimulation

In congestive heart failure, renal blood flow is decreased and renal vascular resistance is increased in a setting of increased activity of both the sympathetic nervous and renin-angiotensin systems. The renal vasoconstrictor response to renal nerve stimulation is enhanced. This is associated with an abnormality in the low-pass filter function of the renal vasculature wherein higher frequencies (≥0.01 Hz) within renal sympathetic nerve activity are not normally attenuated and are passed into the renal blood flow signal. This study tested the hypothesis that excess angiotensin II action mediates the abnormal frequency response characteristics of the renal vasculature in congestive heart failure. In anesthetized rats, the renal vasoconstrictor response to graded frequency renal nerve stimulation was significantly greater in congestive heart failure than in control rats. Losartan attenuated the renal vasoconstrictor response to a significantly greater degree in congestive heart failure than in control rats. In control rats, the frequency response of the renal vasculature was that of a first order (–20 dB/frequency decade) low-pass filter with a corner frequency (–3 dB, 30% attenuation) of 0.002 Hz and 97% attenuation (–30 dB) at ≥0.1 Hz. In congestive heart failure rats, attenuation did not exceed 45% (–5 dB) over the frequency range of 0.001–0.6 Hz. The frequency response of the renal vasculature was not affected by losartan treatment in control rats but was completely restored to normal by losartan treatment in congestive heart failure rats. The enhanced renal vasoconstrictor response to renal nerve stimulation and the associated abnormality in the frequency response characteristics of the renal vasculature seen in congestive heart failure are mediated by the action of angiotensin II on renal angiotensin II AT1 receptors.

Impaired neurogenic control of renal vasculature in renal hypertensive rats

1980 ◽  
Vol 238 (6) ◽  
pp. H770-H775 ◽  
Author(s):  
G. D. Fink ◽  
M. J. Brody
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Innervation ◽  
Renal Hypertension ◽  
Renal Nerves ◽  
Hypertensive Rats ◽  
Renal Vasculature ◽  
Renal Nerve ◽  
Renal Nerve Stimulation ◽  
Renal Vascular ◽  
Renal Sympathetic

Renal hypertension is accompanied by alterations in the renal sympathetic innervation involving reduced catecholamine content and histofluorescence. Because the renal nerves are a potentially important factor in the pathogenesis of renal hypertension, the functional significance of renal catecholamine depletion was evaluated. In rats with either one-kidney or two-kidney Grollman hypertension, renal vascular responses to renal nerve stimulation and intraarterial administration of vasoactive hormones were assessed in vivo at various times following renal compression. In the wrapped kidney of one-kidney hypertensive rats, vasoconstrictor responses to renal nerve stimulation were consistently reduced, compared to responses in uninephrectomized control rats, whereas responses to intra-arterial norepinephrine were slightly greater in kidneys from hypertensive animals. In the untouched kidney of rats with two-kidney renal hypertension, vasoconstrictor responses to nerve stimulation were also substantially reduced, although those to norepinephrine were only slightly altered. It was concluded that catecholamine depletion in the kidneys of renal hypertensive animals reflects a diminished capacity of renal sympathetic nerve impulses to produce vasoconstriction. Reduced neurogenic renal vascular resistance may serve to attenuate the rise in blood pressure in renal hypertension.

NO dependency of RBF and autoregulation in the spontaneously hypertensive rat

2003 ◽  
Vol 285 (1) ◽  
pp. F105-F112 ◽  
Author(s):  
Simona Racasan ◽  
Jaap A. Joles ◽  
Peter Boer ◽  
Hein A. Koomans ◽  
Branko Braam
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Lower Limit ◽  
Vascular Resistance ◽  
Spontaneously Hypertensive Rat ◽  
Renal Vascular Resistance ◽  
Renal Vasculature ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Renal Vascular

In the spontaneously hypertensive rat (SHR), renal blood flow (RBF) has been reported to be very dependent on nitric oxide (NO); however, autoregulation is normal, albeit shifted to higher perfusion pressures. To test the hypothesis that in the SHR NO dependency of RBF autoregulation is diminished, we investigated RBF autoregulation in anesthetized young male SHR and normotensive Wistar-Kyoto (WKY) rats before and during acute intravenous NO synthase (NOS) inhibition with Nω-nitro-l-arginine (l-NNA) and urinary excretion of nitrate plus nitrite (UNOxV) at different renal perfusion pressures (RPP). Under baseline conditions, SHR had higher mean arterial pressure (147 ± 4 mmHg) and renal vascular resistance (16 ± 1 U) than WKY (105 ± 4 mmHg and 10 ± 0.5 U, respectively, P < 0.05). RBF was similar (9.4 ± 0.5 vs. 10.3 ± 0.1 ml · min-1 · g kidney wt-1). Acute NOS blockade increased mean arterial pressure similarly, but there was significantly more reduction in RBF and hence an enhanced increase in renal vascular resistance in SHR (to 36 ± 3 vs. 17 ± 1 U in WKY, P < 0.001). The renal vasculature of SHR is thus strongly dependent on NO in maintaining basal RBF. The lower limit of autoregulation was higher in SHR than WKY in the baseline situation (85 ± 3 vs. 71 ± 2 mmHg, P < 0.05). Acute l-NNA administration did not decrease the lower limit in the SHR (to 81 ± 3 mmHg, not significant) and decreased the lower limit to 63 ± 2 mmHg ( P < 0.05) in the WKY. The degree of compensation as a measure of autoregulatory efficiency attained at spontaneous perfusion pressures was comparable in SHR vs. WKY but with a shift of the curve toward higher perfusion pressures in SHR. Acute NOS blockade only increased the degree of compensation in WKY. Remarkably, UNOxV was significantly lower at spontaneous RPP in SHR. After reduction of RPP, the observed decrease in UNOxV was significantly more pronounced in WKY than in SHR. In conclusion, the renal circulation in SHR is dependent on high levels of NO; however, the capacity to modulate NO in response to RPP-induced changes in shear stress seems to be limited.

Endothelial nitric oxide synthase is predominantly involved in angiotensin II modulation of renal vascular resistance and norepinephrine release

2008 ◽  
Vol 294 (2) ◽  
pp. R421-R428 ◽  
Author(s):  
Johannes Stegbauer ◽  
Yvonne Kuczka ◽  
Oliver Vonend ◽  
Ivo Quack ◽  
Lorenz Sellin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Wild Type ◽  
Norepinephrine Release ◽  
Renal Nerve ◽  
Sympathetic Neurotransmission ◽  
Pressor Responses ◽  
Renal Vascular

Nitric oxide (NO) is mainly generated by endothelial NO synthase (eNOS) or neuronal NOS (nNOS). Recent studies indicate that angiotensin II generates NO release, which modulates renal vascular resistance and sympathetic neurotransmission. Experiments in wild-type [eNOS(+/+) and nNOS(+/+)], eNOS-deficient [eNOS(−/−)], and nNOS-deficient [nNOS(−/−)] mice were performed to determine which NOS isoform is involved. Isolated mice kidneys were perfused with Krebs-Henseleit solution. Endogenous norepinephrine release was measured by HPLC. Angiotensin II dose dependently increased renal vascular resistance in all mice species. EC50 and maximal pressor responses to angiotensin II were greater in eNOS(−/−) than in nNOS(−/−) and smaller in wild-type mice. The nonselective NOS inhibitor Nω-nitro-l-arginine methyl ester (l-NAME; 0.3 mM) enhanced angiotensin II-induced pressor responses in nNOS(−/−) and wild-type mice but not in eNOS(−/−) mice. In nNOS(+/+) mice, 7-nitroindazole monosodium salt (7-NINA; 0.3 mM), a selective nNOS inhibitor, enhanced angiotensin II-induced pressor responses slightly. Angiotensin II-enhanced renal nerve stimulation induced norepinephrine release in all species. l-NAME (0.3 mM) reduced angiotensin II-mediated facilitation of norepinephrine release in nNOS(−/−) and wild-type mice but not in eNOS(−/−) mice. 7-NINA failed to modulate norepinephrine release in nNOS(+/+) mice. (4-Chlorophrnylthio)guanosine-3′, 5′-cyclic monophosphate (0.1 nM) increased norepinephrine release. mRNA expression of eNOS, nNOS, and inducible NOS did not differ between mice strains. In conclusion, angiotensin II-mediated effects on renal vascular resistance and sympathetic neurotransmission are modulated by NO in mice. These effects are mediated by eNOS and nNOS, but NO derived from eNOS dominates. Only NO derived from eNOS seems to modulate angiotensin II-mediated renal norepinephrine release.

scholarly journals Effect of angiotensin II on renal nerve stimulation-induced norepinephrine release in dogs

1987 ◽  
Vol 43 ◽  
pp. 96
Author(s):  
Toshiyuki Matsuoka ◽  
Yoshiharu Hayashi ◽  
Mizue Suzuki-Kusaba ◽  
Susumu Satoh
Keyword(s):  
Angiotensin Ii ◽  
Nerve Stimulation ◽  
Norepinephrine Release ◽  
Renal Nerve ◽  
Renal Nerve Stimulation
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