Contralateral Natriuresis During Reduced Renal Artery Perfusion Pressure in "Renin-Depleted" Dogs

The mechanism of contralateral natriuresis subsequent to reduction of renal perfusion pressure was studied. In control dogs a drop in the renal perfusion pressure caused a very significant increase in the arterial and renal venous plasma renin activity, as well as a significant contralateral natriuresis. Systemic blood pressure increased along with contralateral intrarenal resistance. Glomerular filtration rate and renal blood flow did not change in the opposite kidney.In "renin-depleted" dogs a comparable drop in the renal perfusion pressure failed to stimulate renal venous and arterial plasma renin activity. Contralateral natriuresis increased significantly as well as the systemic blood pressure. In the absence of renin, intrarenal resistance of the opposite kidney did not change. Contralateral glomerular filtration rate and renal blood flow remained unchanged.During reduction of renal perfusion pressure, the most significant findings were: (1) absence of renin release despite the stimulation in renin-depleted dogs, (2) increase in contralateral resistance explained by the renin–angiotensin system, (3) systemic blood pressure increment despite renin release inhibition, and (4) the renin–angiotensin system not directly responsible for the contralateral natriuresis following a reduction in the renal perfusion pressure.Contralateral natriuresis cannot be explained by changes in glomerular filtration, renal blood flow, or intrarenal resistance. It is suggested that the rise in blood pressure or another factor, possibly neural or humoral, could explain the contralateral natriuresis.

Download Full-text

Altered renal hemodynamics and impaired myogenic responses in the fawn-hooded rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.3.r855 ◽

1999 ◽

Vol 276 (3) ◽

pp. R855-R863 ◽

Cited By ~ 30

Author(s):

Richard P. E. van Dokkum ◽

Cheng-Wen Sun ◽

Abraham P. Provoost ◽

Howard J. Jacob ◽

Richard J. Roman

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Renal Blood Flow ◽

Renal Damage ◽

Perfusion Pressure ◽

Renal Perfusion ◽

Myogenic Response ◽

Renal Perfusion Pressure ◽

Medullary Blood Flow ◽

Low Blood Pressure

The present study examined whether an abnormality in the myogenic response of renal arterioles that impairs autoregulation of renal blood flow (RBF) and glomerular capillary pressure (PGC) contributes to the development of renal damage in fawn-hooded hypertensive (FHH) rats. Autoregulation of whole kidney, cortical, and medullary blood flow and PGC were compared in young (12 wk old) FHH and fawn-hooded low blood pressure (FHL) rats in volume-replete and volume-expanded conditions. Baseline RBF, cortical and medullary blood flow, and PGCwere significantly greater in FHH than in FHL rats. Autoregulation of renal and cortical blood flow was significantly impaired in FHH rats compared with results obtained in FHL rats. Myogenically mediated autoregulation of PGC was significantly greater in FHL than in FHH rats. PGC rose from 46 ± 1 to 71 ± 2 mmHg in response to an increase in renal perfusion pressure from 100 to 150 mmHg in FHH rats, whereas it only increased from 39 ± 2 to 53 ± 1 mmHg in FHL rats. Isolated perfused renal interlobular arteries from FHL rats constricted by 10% in response to elevations in transmural pressure from 70 to 120 mmHg. In contrast, the diameter of vessels from FHH rats increased by 15%. These results indicate that the myogenic response of small renal arteries is altered in FHH rats, and this contributes to an impaired autoregulation of renal blood flow and elevations in PGC in this strain.

Download Full-text

Renal autoregulation of blood flow and filtration rate in the rabbit

AJP Renal Physiology ◽

10.1152/ajprenal.1979.237.6.f479 ◽

1979 ◽

Vol 237 (6) ◽

pp. F479-F482 ◽

Cited By ~ 3

Author(s):

C. E. Ott ◽

R. C. Vari

Keyword(s):

Blood Flow ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Filtration Rate ◽

Pressure Range ◽

Perfusion Pressure ◽

Renal Perfusion ◽

Rabbit Kidney ◽

Renal Perfusion Pressure

Electromagnetic flow techniques and inulin clearance were used to determine the autoregulatory capabilities of the rabbit kidney in vivo. Renal blood flow was measured in 13 animals over a renal perfusion pressure range of 40–110 mmHg. Normal renal blood flow averaged 3.2 +/- 0.3 ml.min-1.g kidney-1 and was efficiently autoregulated above a renal artery pressure of 75 mmHg. For every 10 mmHg renal pressure change above 75 mmHg renal blood flow changed only 0.96%. Renal perfusion pressure was reduced from 102 +/- 3 to 74 +/- 2 mmHg in six animals. Over this pressure range glomerular filtration rate was not significantly decreased and averaged 4.2 +/- 0.5 ml/min at high pressure compared to 4.0 +/- 0.5 ml/min at low perfusion pressure. Results show that the rabbit kidney autoregulates renal blood flow and glomerular filtration rate efficiently above 75 mmHg. This range of autoregulation compares well with the autoregulatory range of the dog. The results also show that in the autoregulatory range the rabbit and the rat appear to autoregulate with equal efficiency but that the rabbit kidney begins to autoregulate at a low perfusion pressure than the average of approximately 100 mmHg usually found in the rat.

Download Full-text

Autoregulation of renal blood flow and glomerular filtration rate in the pregnant rabbit

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1987.252.1.r69 ◽

1987 ◽

Vol 252 (1) ◽

pp. R69-R72 ◽

Cited By ~ 5

Author(s):

L. L. Woods ◽

H. L. Mizelle ◽

J. E. Hall

Keyword(s):

Blood Flow ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Filtration Rate ◽

Perfusion Pressure ◽

Renal Perfusion ◽

Renal Perfusion Pressure ◽

Pregnant Rabbit ◽

In Pregnancy

Our purpose was to determine whether renal autoregulatory capability is retained in pregnancy despite the marked renal vasodilation that occurs at this time. Renal blood flow and glomerular filtration rate (GFR) were measured in anesthetized pregnant (22–27 days gestation) and nonpregnant rabbits during step reductions in renal perfusion pressure from control (100 +/- 3 mmHg) to 50 mmHg. Control renal blood flow and GFR were significantly higher in pregnant animals, averaging 65 +/- 5 and 13.1 +/- 1.1 ml/min, respectively, compared with 50 +/- 5 and 9.4 +/- 1.2 ml/min in nonpregnant rabbits. Filtration fraction was also significantly elevated in pregnant animals (0.33 +/- 0.02 vs. 0.27 +/- 0.01 in nonpregnant rabbits). During step reductions in renal perfusion pressure, renal blood flow was well autoregulated down to approximately 70 mmHg in both nonpregnant and pregnant animals, falling by only 9 +/- 4 and 12 +/- 5%, respectively. Likewise, GFR was also well autoregulated, falling by 10 +/- 2 and 8 +/- 3% in nonpregnant and pregnant animals, respectively, when perfusion pressure was reduced from 90 to 70 mmHg. These results suggest that renal autoregulation is preserved in pregnancy despite the fact that the renal circulation is already markedly vasodilated.

Download Full-text

Endothelium modulates renal blood flow but not autoregulation

AJP Renal Physiology ◽

10.1152/ajprenal.1992.262.6.f943 ◽

1992 ◽

Vol 262 (6) ◽

pp. F943-F949 ◽

Cited By ~ 27

Author(s):

W. H. Beierwaltes ◽

D. H. Sigmon ◽

O. A. Carretero

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Renal Blood Flow ◽

Perfusion Pressure ◽

Pressor Response ◽

Renal Perfusion ◽

Systemic Resistance ◽

Renal Vasculature ◽

Lower Flow ◽

Renal Perfusion Pressure

Inhibition of the production of the endothelium-derived relaxing factor (EDRF) nitric oxide using N omega-nitro-L-arginine methyl ester (L-NAME) increases blood pressure (BP) and decreases renal blood flow (RBF), suggesting that basal EDRF can modulate both systemic resistance and renal perfusion. We tested whether L-NAME inhibition of EDRF could also change the autoregulation of RBF. Blood pressure and RBF were measured in Inactin-anesthetized Sprague-Dawley rats. A bolus of 10 mg/kg body wt of L-NAME produced the maximum pressor response (23 +/- 3 mmHg) and blocked acetylcholine-induced renal vasodilation. In control rats, sequential changes in renal perfusion pressure showed that RBF was well autoregulated down to 95 +/- 2 mmHg. L-NAME increased BP, decreased RBF by 33% (P less than 0.005), and increased renal vascular resistance twofold. Although RBF was decreased, the kidney was still able to autoregulate RBF, although reset around the lower flow. Acute hypertension by carotid occlusion and vagotomy increased BP by 26 +/- 6 mmHg (P less than 0.005) and slightly increased RBF, while autoregulation was maintained. The pressor response to L-NAME was amplified to 38 +/- 6 mmHg (P less than 0.001), but RBF decreased by 35% (P less than 0.01). Autoregulation of RBF was maintained, although reset around the lower flow. We conclude that, although endothelial EDRF production may help maintain RBF, it does not seem to mediate the intrinsic autoregulatory responses of the renal vasculature to altered renal perfusion pressure.

Download Full-text

Effect of Hypoxia and Hypercapnic Acidosis on Renal Autoregulation in the Dog: Role of Renal Nerves

Clinical Science ◽

10.1042/cs0650533 ◽

1983 ◽

Vol 65 (5) ◽

pp. 533-538 ◽

Cited By ~ 6

Author(s):

Robert J. Anderson ◽

Richard G. Pluss ◽

William T. Pluss ◽

Jon Bell ◽

Gary G. Zerbe

Keyword(s):

Blood Flow ◽

Glomerular Filtration Rate ◽

Glomerular Filtration ◽

Renal Blood Flow ◽

Filtration Rate ◽

Perfusion Pressure ◽

Renal Perfusion ◽

Renal Nerves ◽

Hypercapnic Acidosis ◽

Renal Perfusion Pressure

1. Previous studies suggest that hypoxia and hypercapnic acidosis exert a renal nerve mediated adverse effect on renal haemodynamic function. We therefore examined the effect of hypoxia and hypercapnic acidosis on renal blood flow and glomerular filtration rate responses to lowering renal perfusion pressure from 125 to 75 mmHg in the anaesthetized dog. To study the role of renal nerves in these responses, paired innervated and denervated kidneys were studied in each animal. 2. Hypoxia (Po2 43 ± 3 mmHg) affected neither renal blood flow nor glomerular filtration rate responses to decreasing renal perfusion pressure. 3. Hypercapnic acidosis (Pco2 71 ±2 mmHg; pH 7.03 ± 0.01) significantly decreased both renal blood flow and glomerular filtration rate as renal perfusion pressure was lowered. This effect of hypercapnic acidosis could be abolished by renal denervation. 4. These findings suggest that hypercapnic acidosis results in renal nerve stimulation, which prevents the usual decrease in renal afferent arteriolar tone that occurs in response to lowering of renal perfusion pressure.

Download Full-text

Directly measuring spinal cord blood flow and spinal cord perfusion pressure via the collateral network: Correlations with changes in systemic blood pressure

Journal of Thoracic and Cardiovascular Surgery ◽

10.1016/j.jtcvs.2014.09.121 ◽

2015 ◽

Vol 149 (1) ◽

pp. 360-366 ◽

Cited By ~ 14

Author(s):

Yuya Kise ◽

Yukio Kuniyoshi ◽

Hitoshi Inafuku ◽

Takaaki Nagano ◽

Tsuneo Hirayasu ◽

...

Keyword(s):

Blood Pressure ◽

Spinal Cord ◽

Blood Flow ◽

Cord Blood ◽

Perfusion Pressure ◽

Systemic Blood Pressure ◽

Spinal Cord Blood Flow ◽

Systemic Blood ◽

Collateral Network

Download Full-text

Plasma renin activity responses to graded decreases in renal perfusion pressure in fetal and newborn lambs

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1992.262.3.r524 ◽

1992 ◽

Vol 262 (3) ◽

pp. R524-R529 ◽

Cited By ~ 7

Author(s):

N. D. Binder ◽

D. F. Anderson

Keyword(s):

Blood Pressure ◽

Plasma Renin Activity ◽

Perfusion Pressure ◽

Plasma Renin ◽

Renal Perfusion ◽

Renin Activity ◽

Renal Perfusion Pressure ◽

Arterial Blood ◽

The Right ◽

The Relationship

We examined the relationship between acute reductions in renal perfusion pressure, as approximated by femoral arterial blood pressure, and plasma renin activity in the uninephrectomized fetal lamb. Renal perfusion pressure was reduced and maintained at a constant value by controlled partial occlusion of the aorta above the renal artery. After 15 min of reduced blood pressure, blood samples were taken for determination of plasma renin activity. This protocol was performed 22 times in 11 fetal lambs. Additionally, three of the fetuses were delivered by cesarean section and studied as newborns for the first week of life. In the fetus, there was a linear relationship between log plasma renin activity and femoral arterial blood pressure (P less than 0.01). After birth, the relationship still existed, although it was shifted to the right (P less than 0.0001). We conclude that there is a significant relationship between plasma renin activity and renal perfusion pressure in the fetal lamb, and as early as 1 day after birth, this relationship shifts to the right in the newborn lamb.

Download Full-text

Mechanism of intrarenal blood flow redistribution after carotid artery occlusion

AJP Renal Physiology ◽

10.1152/ajprenal.1977.232.2.f167 ◽

1977 ◽

Vol 232 (2) ◽

pp. F167-F172 ◽

Cited By ~ 1

Author(s):

E. H. Prosnitz ◽

E. J. Zambraski ◽

G. F. DiBona

Keyword(s):

Blood Flow ◽

Carotid Artery ◽

Renal Blood Flow ◽

Perfusion Pressure ◽

Renal Perfusion ◽

Artery Occlusion ◽

Carotid Artery Occlusion ◽

Outer Cortex ◽

Renal Sympathetic Nerve Activity ◽

Renal Perfusion Pressure

Bilateral carotid artery occlusion results in an increase in mean arterial pressure, an increase in renal sympathetic nerve activity, and a redistribution of renal blood flow from inner to outer cortex. To elucidate the mechanism of the renal blood flow redistribution, carotid artery occlusion was performed in anesthetized dogs with the left kidney either having renal perfusion pressure maintained constant (aortic constriction) or having alpha-adrenergic receptor blockade (phenoxybenzamine); the right kidney of the same dog served to document the normal response. When renal perfusion pressure was maintained constant, renal blood flow distribution (microspheres) was unchanged by carotid artery occlusion. In the presence of renal alpha-adrenergic receptor blockade, carotid artery occlusion elicited the usual redistribution of renal blood flow from inner to outer cortex. The redistribution of renal blood flow observed after carotid artery occlusion is mediated by the increase in renal perfusion pressure rather than the increase in renal sympathetic nerve activity.

Download Full-text