Renal vascular reactivity to U 46619 and adrenergic agonists in Goldblatt hypertension

1987 ◽  
Vol 253 (6) ◽  
pp. H1523-H1529 ◽  
Author(s):  
B. G. Zimmerman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Adrenergic Agonists ◽  
Contralateral Kidney ◽  
Beta Adrenoceptor ◽  
Arterial Blood ◽  
Arterial Plasma ◽  
Renal Vascular ◽  
Goldblatt Hypertension

Vascular reactivity of the contralateral kidney of conscious Goldblatt hypertensive dogs was studied by eliciting renal blood flow (RBF) responses to intra-arterial infusions of vasoconstrictor and vasodilator agonists in control sessions and at weekly intervals postclipping. Systemic arterial blood pressure (BP) and RBF were monitored during each recording session via an implanted catheter and electromagnetic blood flow probe, respectively. BP was maximally increased within 1 wk and remained elevated for the duration of the study. The relationship between the negative percent change in RBF (-% delta RBF) and the renal arterial plasma concentration of adrenergic agonists, angiotensin II and thromboxane mimetic (U 46619), infused intra-arterially was subjected to regression analysis, and 25 and 50% effective doses (ED25 and ED50, respectively) were calculated. Vascular sensitivity to phenylephrine and norepinephrine increased within a month or more of hypertension. Vascular reactivity to angiotensin II was unchanged. In contrast to the delayed increase in renal vascular reactivity to adrenergic agonists, enhancement of the RBF responses to U 46619 was seen within 1-2 wk. In addition, beta-adrenoceptor-mediated vasodilation appeared suppressed during hypertension. Alteration in the response of the contralateral kidney to both vasoconstrictor and beta-adrenoceptor-mediated vasodilator stimuli may contribute to renal hemodynamic changes in Goldblatt hypertension.

Renal hemodynamics and vascular reactivity in canine DOCA-salt hypertension

1988 ◽  
Vol 255 (4) ◽  
pp. R563-R568
Author(s):  
J. L. Goering ◽  
P. C. Raich ◽  
B. G. Zimmerman
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Tone ◽  
Vascular Reactivity ◽  
Control Period ◽  
Indwelling Catheter ◽  
Alpha Adrenoceptor ◽  
Arterial Blood ◽  
Salt Hypertension ◽  
Renal Vascular

Because of the potential role that the kidney may play in deoxycorticosterone acetate (DOCA)-salt hypertension, changes in renal blood flow, renal vascular reactivity, and renal adrenergic vascular tone were followed in the conscious instrumented dog. DOCA-salt was administered daily after obtaining control measurements. Systemic mean arterial blood pressure (MAP) was monitored with an indwelling catheter, renal blood flow (RBF) was measured electromagnetically using an implanted blood flow probe, and drugs were administered intrarenal arterially through an indwelling renal artery catheter. During the first week of DOCA-salt administration MAP increased from 106 +/- 3 to 118 +/- 2 mmHg and at week 2 to 123 +/- 2 mmHg (P less than 0.01). RBF increased from 275 +/- 32 to 336 +/- 34 during week 1 (P less than 0.05) and to 324 +/- 29 ml/min during week 2. The log ED50 of norepinephrine administered intra-arterially decreased from 1.66 +/- 0.114 to 1.48 +/- 0.091 and 1.41 +/- 0.067 ng/ml (P less than 0.05), and of angiotensin II from 2.58 +/- 0.072 to 2.31 +/- 0.09 (P less than 0.05) and 2.38 +/- 0.05 pg/ml, during weeks 1 and 2, respectively. There was, however, no increase in adrenergic vascular tone as determined by the change in RBF obtained with the intra-arterial infusion of alpha-adrenoceptor antagonists. These experiments indicate that RBF is not compromised in canine DOCA-salt hypertension, and renal adrenergic tone is no greater in the hypertensive than in the normotensive control period.

Cyclosporine augments renal but not systemic vascular reactivity

1990 ◽  
Vol 258 (1) ◽  
pp. F211-F217
Author(s):  
M. D. Garr ◽  
M. S. Paller
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Arginine Vasopressin ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Vascular Responsiveness ◽  
Renal Vascular

Renal vasoconstriction and hypertension are major side effects of cyclosporine. We tested the acute effects of cyclosporine on renal and systemic vascular reactivity to norepinephrine, angiotensin II, and arginine vasopressin. Renal vascular reactivity was tested in anesthetized Sprague-Dawley rats with denervated kidneys. Renal blood flow was measured with an electromagnetic flow probe in response to graded intra-arterial infusions of vasoconstrictors before and after intravenous administration of cyclosporine. Cyclosporine augmented the decrease in renal blood flow and the increase in renal vascular resistance produced by intrarenal norepinephrine, angiotensin II, and arginine vasopressin. In these studies, systemic blood pressure did not change and cyclosporine caused no direct change in basal renal blood flow. In contrast, in conscious animals, cyclosporine did not increase the pressor response to intravenous norepinephrine or to angiotensin II. Rather, cyclosporine caused enhanced baroreflex slowing of heart rate and a decrease in the pressor response to both norepinephrine and angiotensin II. Even when the baroreceptor reflex was blocked by pentolinium, the pressor response to norepinephrine in cyclosporine-treated animals was diminished compared with vehicle-treated animals. Therefore, although cyclosporine augmented renal vasoconstriction in response to norepinephrine, angiotensin II, and arginine vasopressin, it did not acutely increase the systemic vascular response to these agents. Enhanced renal vascular responsiveness is an additional mechanism for cyclosporine-mediated renal vasoconstriction. Lack of enhanced peripheral vascular responsiveness suggests that hypertension is not likely to be due to direct effects on the systemic vasculature and is more likely to be a consequence of renal functional impairment.

Inhibition by Bradykinin of the Vascular Effects of Pressor Hormones in the Canine Kidney: Relationship to Prostaglandins

1980 ◽  
Vol 59 (s6) ◽  
pp. 145s-148s ◽  
Author(s):  
H. Sušić ◽  
A. Nasjletti ◽  
K. U. Malik
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Vascular Reactivity ◽  
Sodium Pentobarbital ◽  
Vascular Effects ◽  
Arterial Infusion ◽  
Renal Vasoconstriction ◽  
Renal Vascular ◽  
Canine Kidney

1. Renal arterial injection of bolus doses of angiotensin II or noradrenaline, (0.06, 0.12 and 0.25 μg) caused renal vasoconstriction and decreased blood flow to the kidney in a dose-related manner in dogs anaesthetized by sodium pentobarbital. 2. The effect of angiotensin II and noradrenaline in lowering renal blood flow was reduced during renal arterial infusion of either bradykinin (10 ng min−1 kg−1) or prostaglandin E2 (4 ng min−1 kg−1). 3. Pretreatment of the dogs with an inhibitor of prostaglandin synthesis, sodium meclofenamate (5 mg/kg), blunted the inhibitory action of bradykinin, but not that of prostaglandin E2, on renal vascular reactivity to angiotensin II and noradrenaline. 4. These results indicate that bradykinin reduces the renal vasoconstriction induced by angiotensin II and noradrenaline in the dog by a mechanism dependent upon synthesis of prostaglandins.

Impaired Autoregulatory Responses in Contralateral Kidneys of Two-Kidney, One-Clip Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 381s-384s ◽  
Author(s):  
D. W. Ploth ◽  
R. N. Roy ◽  
Wann-Chu Huang ◽  
L. G. Navar
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Urine Flow ◽  
Renal Vascular Resistance ◽  
Hypertensive Rats ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Vascular

1. Micropuncture and clearance experiments in two-kidney, one-clip renal vascular hypertensive rats examined the ability of the kidney contralateral to renal vascular stenosis to maintain renal function during conditions of reduced renal arterial blood pressure. 2. At their respective spontaneous blood pressures, renal vascular resistance was higher and glomerular filtration rate (GFR) and renal blood flow were not different in the contralateral kidneys of the hypertensive rats (170 ± 5 mmHg) compared with normal animals (129 ± 1 mmHg). Urine flow and absolute and fractional excretion of electrolyte were greater from the kidneys of the hypertensive animals. However, pressures in cortical structures were similar in the two groups. 3. As blood pressure was reduced acutely, the kidney contralateral to the renal artery stenosis achieved only small decreases in renal vascular resistance that failed to allow GFR, renal blood flow or pressures in cortical structures to be maintained. In contrast, normal rats efficiently autoregulated renal vascular resistance to allow GFR, renal blood flow and cortical pressures to be unchanged as blood pressure was altered between 130 and 115 mmHg. Urine flow and electrolyte excretion decreased to a greater extent in the hypertensive kidneys; at comparable blood pressure these indices of excretory function were not different in the two groups. 4. These observations indicate that the contralateral kidney can maintain normal haemodynamic and glomerular function only at elevated blood pressure and suggest the possibility that the impaired capacity to autoregulate renal resistances may contribute to the maintenance of hypertension observed in this model.

Exaggerated renal vascular reactivity to angiotensin and thromboxane in young genetically hypertensive rats

1990 ◽  
Vol 259 (2) ◽  
pp. F372-F382 ◽  
Author(s):  
C. Chatziantoniou ◽  
F. H. Daniels ◽  
W. J. Arendshorst
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Receptor Agonist ◽  
Vascular Reactivity ◽  
Prostaglandin Synthesis ◽  
Genetic Hypertension ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Renal Vascular

The objective of this study was to test the hypothesis that angiotensin II and thromboxane A2 (TxA2) contribute to the elevated renal vascular resistance observed during the development of genetic hypertension. In 6-wk-old anesthetized spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats, renal blood flow (electromagnetic flowmetry) and carotid arterial pressure were measured during bolus injections of different doses of angiotensin II and U46619 (stable receptor agonist of TxA2) into the renal artery before and during inhibition of prostaglandin synthesis by indomethacin. In all cases, arterial pressure remained unchanged at the pre-injection levels. Under control conditions, angiotensin II reduced renal blood flow in SHR almost twice as much as in WKY. This strain difference was abolished by inhibition of prostaglandin synthesis, suggesting that a deficiency in the action of endogenous vasodilator prostaglandins is responsible for the enhanced response to angiotensin II in SHR. Under control conditions, the TxA2-receptor agonist produced similar reductions of renal blood flow in SHR and WKY. However, after indomethacin, the agonist-induced vasoconstriction was twice as large in SHR as in WKY, suggesting that SHR kidneys have an increased vascular reactivity to TxA2, which is unmasked when indomethacin reduces elevated levels of endogenous TxA2. These findings indicate important strain differences between young SHR and WKY in the renal vascular response to angiotensin II and TxA2 that may contribute to the renal vasoconstriction observed during the development of genetic hypertension.

Vascular reactivity to angiotensin II in the normotensive and hypertensive pregnant ewe

1980 ◽  
Vol 238 (2) ◽  
pp. H209-H213
Author(s):  
S. M. Lieb ◽  
T. Cabalum ◽  
M. Zugaib ◽  
R. Erkkola ◽  
K. Tabsh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Renal Hypertension ◽  
Circulatory Response ◽  
Pregnant Sheep ◽  
Experimental Renal Hypertension ◽  
Pregnant Ewe ◽  
Renal Vascular

The circulatory responses to progressively increasing doses of angiotensin II were studied in the same group of chronically instrumented unanesthetized pregnant sheep during three consecutive periods: a) normotensive with intact kidneys; b) normotensive with unilateral nephrectomy; and c) one-kidney hypertension. The results show that 1) the pressor response to a given dose of angiotensin was significantly greater in the normotensive than in the hypertensive condition; 2) uterine blood flow decreased markedly with the development of hypertension; 3) uterine circulatory response to angiotensin depended on the dosage; the response was less the the hypertensive than in the normotensive condition; 4) renal blood flow decreased and renal vascular resistance increased during angiotensin infusion, but the response was less in the hypertensive than in the normotensive condition; the response of the renal circulation decreased with increasing doses of angiotensin. These observations suggest a generalized vascular refractoriness to exogenous angiotensin II in the pregnant ewe with experimental renal hypertension.

Effect of [Sar1, Ala8]angiotensin II on renal vascular resistance

1975 ◽  
Vol 229 (3) ◽  
pp. 640-645 ◽  
Author(s):  
S Satoh ◽  
BG Zimmerman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Systemic Blood Pressure ◽  
Renal Vascular Resistance ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Contralateral Kidney ◽  
Anesthetized Dogs ◽  
Renal Vascular

Partial occlusion of the renal artery (RAO) was induced in dogs anesthetized with pentobarbital or morphine chloralose-urethan. The effect of [Sar1, Ala8]angiotensin II (P-113) was compared before and during RAO on blood flow and vascular resistance of the contralateral kidney. An increase in renin secretion rate was obtained in the ischemic kidney, which was accompanied by an increase in renal vascular resistance (RVR) in the contralateral kidney and a rise in systemic blood pressure. P-113 given intra-arterially to the contralateral kidney consistently increased renal blood flow and decreased RVR during RAO, but did not alter RVR significantly before RAO. The elevation in renin secretion rate decreased between 30 and 122 min after the initiation of RAO in the pentobarbital-anesthetized dogs but not in the chloralose-urethan-anesthetized dogs. These experiments indicate that during RAO release of renin causes, through formation of angiotensin, an increase in RVR in the contralateral kidney and intra-arterial administration of P-113 restores the vascular resistance to a near-normal level.

Renal blood flow changes in contralateral kidney of Goldblatt hypertensive dog

1981 ◽  
Vol 241 (2) ◽  
pp. H145-H148
Author(s):  
B. G. Zimmerman ◽  
C. Mommsen
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Control Level ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Vascular

Sequential changes in systemic arterial blood pressure (BP), renal blood flow (RBF) in the contralateral kidney, and plasma renin activity (PRA) were examined on conscious dogs with construction of a single renal artery (RAC). An increase of 24 mmHg in bP occurred within 2 days after RAC, and BP later plateaued at a lower level. RBF in the contralateral kidney transiently increased by 24% and then returned to the control level in 11-14 days. PRA also peaked early after RAC and then returned to control. The clamp was tightened and the renal artery was occluded (RAO) 3-20 days after RAC. BP, RBF, and PRA increased to an even greater degree than after RAC. BP peaked at 145 mmHg, and RBF increased 61.5% at 2-3 days after RAO. BP and RBF both decreased but remained above the control for the duration of the study, BP at 127 mmHg and RBF at 256 ml/min. RBF per gram for the hypertrophied contralateral kidney was calculated from the RBF before death and the weight at death. The final RBF per gram of the contralateral kidney (2.7 ml.min-1.g-1) decreased and renal vascular resistance increased compared with the estimated control RBF/g (3.7 ml.min-1.g-1) and renal vascular resistance. These results suggest that the final RBF of the contralateral kidney is not increased in proportion to its increase in weight and that it may be relatively hypoperfused in two-kidney one-clip Goldblatt hypertension.

Vascular reactivity of contralateral kidney in awake Goldblatt hypertensive dog

1986 ◽  
Vol 250 (6) ◽  
pp. H1043-H1049
Author(s):  
B. G. Zimmerman
Keyword(s):  
Plasma Renin Activity ◽  
Vascular Reactivity ◽  
Plasma Renin ◽  
Control Session ◽  
Ang Ii ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Group 2 ◽  
Renal Vascular ◽  
Group 1

Sixteen dogs were instrumented for recording mean arterial blood pressure (MAP) and blood flow from the left renal artery (RBF) and for intra-arterial infusions of norepinephrine (NE) and angiotensin II (ANG II). Nine dogs (group 1) were studied while normotensive and also when hypertensive. Seven control dogs (group 2) were studied only when normotensive. In a control session conducted in group 1 and at weekly intervals for up to 6-12 wk after the right renal artery was clipped, infusions of NE and ANG II were given intra-arterially to produce graded decreases in RBF. Group 2 was studied similarly in a control session and 4-7 wk later. Regressions of the values of percent change RBF (arc sin transformation) on the concentrations of NE and ANG II in renal arterial blood estimated the renal vascular reactivity of the hypertensives' contralateral kidney and the normotensives' kidney. In group 1, during the postclipping intervals when MAP and plasma renin activity were increased, the renal vascular reactivity to NE, but not to ANG II was increased. This was based on the significant elevation above the X axis in the postclipping regressions. In group 2, MAP, plasma renin activity, and renal vascular reactivity to NE and ANG II were unchanged over the 4- to 7-wk interval of study. These results indicate that the contralateral kidney develops an increased vascular reactivity to NE but not to ANG II in Goldblatt hypertension.

Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Sexually Dimorphic ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Renal Vascular

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.

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