Role of Renal Perfusion Pressure Versus Angiotensin II on Renal Oxidative Stress in Angiotensin II–Induced Hypertensive Rats

An adaptation of the in vitro perfused hydronephrotic rat kidney model allowing in situ measurement of arteriolar membrane potentials is described. At a renal perfusion pressure of 80 mmHg, resting membrane potentials of interlobular arteries (22 +/- 2 microns) and afferent (14 +/- 1 microns) and efferent arterioles (12 +/- 1 microns) were -40 +/- 2 (n = 8), -40 +/- 1 (n = 45), and -38 +/- 2 mV (n = 22), respectively (P = 0.75). Using a dual-pipette system to stabilize the impalement site, we measured afferent and efferent arteriolar membrane potentials during angiotensin II (ANG II)-induced vasoconstriction. ANG II (0.1 nM) reduced afferent arteriolar diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.005) and membrane potentials from -40 +/- 2 to -29 +/- mV (P = 0.012). ANG II elicited a similar vasoconstriction in efferent arterioles, decreasing diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.004), but failed to elicit a significant depolarization (-39 +/- 2 for control; -36 +/- 3 mV for ANG II; P = 0.27). Our findings thus indicate that resting membrane potentials of pre- and postglomerular arterioles are similar and lie near the threshold activation potential for L-type Ca channels. ANG II-induced vasoconstriction appears to be closely coupled to membrane depolarization in the afferent arteriole, whereas mechanical and electrical responses appear to be dissociated in the efferent arteriole.

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Implication of renal perfusion pressure in stroke of spontaneously hypertensive rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1980.238.3.h317 ◽

1980 ◽

Vol 238 (3) ◽

pp. H317-H324 ◽

Cited By ~ 1

Author(s):

A. Nagaoka ◽

A. Shino ◽

M. Shibota

Keyword(s):

Spontaneously Hypertensive Rats ◽

Renal Cortex ◽

Perfusion Pressure ◽

Renal Perfusion ◽

Hypertensive Rats ◽

Cerebrovascular Lesions ◽

Spontaneously Hypertensive ◽

Renal Perfusion Pressure ◽

Renal Changes ◽

Renal Cortical Blood Flow

To elucidate the significance of hypertension associated with cerebrovascular lesions (CVL), renal perfusion pressure (RPP) was controlled by aortic clips of two different sizes in stroke-prone spontaneously hypertensive rats kept under normal or salt-loaded conditions. Tail and femoral arterial pressures (RPPs) in the mildly and severely clamped animals were reduced in proportion to the severity of the clamping. In contrast, carotid pressures in both clamped groups were significantly higher than that in the controls. Proteinuria and hyperreninemia accompanied by arteriolar changes in the renal cortex were observed in the controls prior to the onset of CVL. The renal changes were inhibited by both types of clamping. The onset of CVL was delayed by the mild clamping in salt-loaded animals, but accelerated by the severe clamping in both the normal and salt-loaded animals. Renal cortical blood flow was decreased only by the severe clamping. The results suggest that reduction in RPP and/or renal ischemia, which seems to be due to the hypertensive arteriolar changes in the renal cortex, may be related to the pathogenesis of CVL in the stroke-prone rats with or without hyperreninemia.

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Effects of meclofenamate on the renin response to aortic constriction in the rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1984.247.3.r546 ◽

1984 ◽

Vol 247 (3) ◽

pp. R546-R551 ◽

Cited By ~ 2

Author(s):

D. Villarreal ◽

J. O. Davis ◽

R. H. Freeman ◽

W. D. Sweet ◽

J. R. Dietz

Keyword(s):

Perfusion Pressure ◽

Plasma Renin ◽

Renal Perfusion ◽

Renin Release ◽

Aortic Constriction ◽

Renal Perfusion Pressure ◽

Inhibition Of Prostaglandin Synthesis ◽

Intact Kidney ◽

Stimulus Secretion Coupling

This study examines the role of the renal prostaglandin system in stimulus-secretion coupling for renal baroreceptor-dependent renin release in the anesthetized rat. Changes in plasma renin activity (PRA) secondary to suprarenal aortic constriction were evaluated in groups of rats with a single denervated nonfiltering kidney (DNFK) with and without pretreatment with meclofenamate. Suprarenal aortic constriction was adjusted to reduce renal perfusion pressure to either 100 or 50 mmHg. In addition, similar experiments were performed in rats with a single intact filtering kidney. Inhibition of prostaglandin synthesis with meclofenamate failed to block or attenuate the increase in PRA in response to the decrement in renal perfusion pressure after both severe and mild aortic constriction for both the DNFK and the intact-kidney groups. The adequacy of prostaglandin inhibition was demonstrated by complete blockade with meclofenamate of the marked hypotensive and hyperreninemic responses to sodium arachidonate. The results in the DNFK indicate that in the rat, renal prostaglandins do not function as obligatory mediators of the isolated renal baroreceptor mechanism for the control of renin release. Also the findings in the intact filtering kidney suggest that prostaglandins are not essential in the renin response of other intrarenal receptor mechanisms that also are stimulated by a reduction in renal perfusion pressure.

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Role of the endothelium-dependent relaxing factor nitric oxide on renal function.

Journal of the American Society of Nephrology ◽

10.1681/asn.v291371 ◽

1992 ◽

Vol 2 (9) ◽

pp. 1371-1387 ◽

Cited By ~ 1

Author(s):

J C Romero ◽

V Lahera ◽

M G Salom ◽

M L Biondi

Keyword(s):

Nitric Oxide ◽

Renal Function ◽

Perfusion Pressure ◽

Sodium Intake ◽

Systemic Circulation ◽

Renal Perfusion ◽

Renin Release ◽

High Sodium ◽

Renal Perfusion Pressure

The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.

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Renal perfusion pressure and renin secretion in bilaterally renal denervated sheep

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y94-111 ◽

1994 ◽

Vol 72 (7) ◽

pp. 782-787 ◽

Cited By ~ 10

Author(s):

L. Fan ◽

S. Mukaddam-Daher ◽

J. Gutkowska ◽

B. S. Nuwayhid ◽

E. W. Quillen Jr.

Keyword(s):

Angiotensin Ii ◽

Atrial Natriuretic Factor ◽

Perfusion Pressure ◽

Excretion Rate ◽

Plasma Renin ◽

Renal Perfusion ◽

Renin Secretion ◽

Renal Nerves ◽

Renal Perfusion Pressure ◽

Plasma Angiotensin

To further investigate the influence of renal nerves on renin secretion, the renin secretion responses to step reductions of renal perfusion pressure (RPP) were studied in conscious sheep with innervated kidneys (n = 5) and with bilaterally denervated kidneys (n = 5). The average basal level of RPP in sheep with denervated kidneys (82 ± 4 mmHg; 1 mmHg = 133.3 Pa) was similar to that in sheep with innervated kidneys (83 ± 3 mmHg). RPP was reduced in four sequential 15-min steps, to a final level of 54 ± 2 mmHg in sheep with innervated kidneys and to 57 ± 1 mmHg in denervated sheep. The renin secretion rate was increased as RPP was reduced in sheep with innervated kidneys. Baseline peripheral plasma renin activity was reduced and there was almost no response of renin secretion rate to reduction of RPP in sheep with denervated kidneys. Also, baseline renal blood flow, urine flow rate, sodium excretion rate, and potassium excretion rate were higher in sheep with denervated kidneys than those with innervated kidneys. Baseline plasma angiotensin II was similar in both groups of sheep. As RPP was decreased, plasma angiotensin II was increased in sheep with innervated kidneys, but was not significantly altered in sheep with denervated kidneys. Plasma atrial natriuretic factor was unaltered by either reduction of RPP or renal denervation. In conclusion, hormonal factors, such as angiotensin II and atrial natriuretic factor, do not account for the dramatic suppression of renin secretion in response to the reduction of RPP in sheep with bilateral renal denervation. Renal nerves are a necessary component in the control of renin secretion during reduction of RPP and may contribute to the regulation of baseline plasma renin activity and sodium excretion rate in conscious ewes.Key words: renin secretion, renal perfusion pressure, renal nerves, denervation, sheep.

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ACE inhibition prevents Na and water retention and MABP increase during reduction of renal perfusion pressure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1995.269.3.r481 ◽

1995 ◽

Vol 269 (3) ◽

pp. R481-R489 ◽

Cited By ~ 3

Author(s):

W. Boemke ◽

E. Seeliger ◽

L. Rothermund ◽

M. Corea ◽

R. Pettker ◽

...

Keyword(s):

Angiotensin Ii ◽

Angiotensin Converting Enzyme ◽

Water Retention ◽

Perfusion Pressure ◽

Renal Perfusion ◽

Plasma Aldosterone ◽

Angiotensin Converting Enzyme Inhibition ◽

Converting Enzyme ◽

Renal Perfusion Pressure ◽

Arterial Blood

Two groups of six dogs were studied during 4 control days and 4 days of reduced renal perfusion pressure (rRPP) servo controlled at 20% below the individual dog's 24-h mean arterial blood pressure (MABP) during control days, i.e., below the threshold for renin release. On rRPP days, endogenous activation of plasma aldosterone and angiotensin II was inhibited by the angiotensin-converting enzyme inhibitor captopril. The dogs were kept on a high-Na and high-water intake. Unlike studies during rRPP alone, there was no Na and water retention during rRPP+captopril. Glomerular filtration rate dropped by approximately 9%, and MABP remained in the range of control days. Plasma renin activity rose to values 14 times greater than control, whereas plasma aldosterone decreased by approximately 60%. Atrial natriuretic peptide remained in the range of controls. In conclusion, angiotensin-converting enzyme inhibition can prevent the otherwise obligatory Na and water retention and systemic MABP increase during a 20% reduction in renal perfusion pressure. This is achieved most likely via the captopril-induced fall in angiotensin II and plasma aldosterone levels.

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Role of renal interstitial hydrostatic pressure in the pressure diuresis response

AJP Renal Physiology ◽

10.1152/ajprenal.1989.256.1.f63 ◽

1989 ◽

Vol 256 (1) ◽

pp. F63-F70 ◽

Cited By ~ 19

Author(s):

J. Garcia-Estan ◽

R. J. Roman

Keyword(s):

Hydrostatic Pressure ◽

Sodium Excretion ◽

Perfusion Pressure ◽

Renal Perfusion ◽

Renal Capsule ◽

Interstitial Pressure ◽

Renal Perfusion Pressure ◽

Residual Response

The present study examines the role of renal interstitial hydrostatic pressure (RIHP) in the pressure-diuretic and -natriuretic response. The relationships between RIHP, sodium excretion, and renal perfusion pressure (RPP) were determined in antidiuretic and volume-expanded (VE) rats with an intact or decapsulated kidney. RIHP was measured by use of the implanted capsule technique. RIHP increased significantly from 7.5 +/- 0.8 to 12.0 +/- 1.4 mmHg in VE animals and from 3.3 +/- 0.4 to 5.2 +/- 0.7 mmHg in antidiuretic rats after RPP was varied from 100 to 150 mmHg. The pressure-natriuretic response of the antidiuretic rats was blunted compared with that observed in the VE rats. Decapsulation of the kidney in VE rats lowered RIHP and reduced, but did not eliminate, the pressure-natriuretic response. To determine whether this residual response was related to changes in interstitial pressure in the medulla, cortical (CIHP) and medullary interstitial hydrostatic pressures (MIHP) were simultaneously measured in VE rats with an intact or decapsulated kidney. In control rats CIHP and MIHP were similar at all levels of RPP studied. In rats with the renal capsule removed MIHP was higher than CIHP and rose significantly from 6.7 +/- 0.8 to 9.2 +/- 0.8 mmHg when RPP was varied from 100 to 150 mmHg. These results indicate that pressure diuresis and natriuresis is accompanied by changes in RIHP and the response is modulated by the basal level of RIHP. These findings suggest that changes in MIHP may serve as an intrarenal signal for this response.

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Role of the Renal Nerves in Renin Release during Suprarenal Aortic Stenosis in Cats

Clinical Science ◽

10.1042/cs051085s ◽

1976 ◽

Vol 51 (s3) ◽

pp. 85s-87s

Author(s):

A. Stella ◽

F. Calaresu ◽

A. Zanchetti

Keyword(s):

Aortic Stenosis ◽

Time Course ◽

Perfusion Pressure ◽

Renal Perfusion ◽

Renin Release ◽

Renal Nerves ◽

Renal Perfusion Pressure ◽

The Difference

1. Renin release from an intact, innervated kidney and from the contralateral denervated kidney was measured before and during a period of suprarenal aortic stenosis. 2. Aortic stenosis of 10 min duration reduced renal perfusion pressure to 50 mmHg and increased renin release from both kidneys, but the response from the innervated kidney was greater. 3. A study of the time-course of the response during 30 min of aortic stenosis showed that the difference in rate of renin release between the innervated and the denervated kidney is greatest during the first few minutes of aortic stenosis.

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