Sympathetic and renin-angiotensin system influence on blood pressure and renal blood flow of two-kidney, one clip Goldblatt hypertensive dog.

Zimmerman, Ben G.; Mommsen, Craig; Kraft, E

doi:10.1161/01.hyp.2.1.53

Cited by 25 publications

(9 citation statements)

References 33 publications

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“…It has been suggested that increased activity of the renin-angiotensin system resulting from clipping of one renal artery would be expected to influence the VOL 3, No 3, MAY-JUNE 1981 nonclipped kidney. 11 This has received support from studies demonstrating that administration of angiotensin antagonists reduce the elevated renal vascular resistance in the contralateral kidney; 11 - 13 however, there is little information regarding the individual GFR and excretory responses of the clipped and nonclipped kidneys to blockade of the renin-angiotensin system. Of interest is the unique circumstance occurring in this hypertensive model of a renin-depleted kidney existing in an environment of elevated plasma renin levels.…”

mentioning

confidence: 99%

Bilateral renal function responses to converting enzyme inhibitor (SQ 20,881) in two-kidney, one clip Goldblatt hypertensive rats.

Huang¹,

Ploth²,

Bell³

et al. 1981

Hypertension

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SUMMARYThe influence of the renln-angiotensin system on individual kidney function of two-kidney, one clip Goldblatt hypertensive (GH) rats was evaluated by determining renal functional responses during intravenous infusion of converting enzyme inhibitor (CEI) (SQ 20,881, 0 J rag/100 g-hr) for 3.5 bourn. Rats were made hypertensive by placing a 0.25 mm silver clip on the right renal artery 3-4 weeks prior to study. Normal rats and GH rats were prepared to allow urine collections from each kidney. Mean arterial pressure of GH rats fell significantly from preinfusion levels of 153 ± 7 to 126 ± 4 mm Hg during CEI infusion. Despite this decrease in arterial pressure, the nondipped kidneys with reduced renal renin activity (14 ± 5 vs 293 ± 40 ng Al/mg-hr in the clipped kidney) exhibited dramatic increases in gtomerular filtration rate (GFR) (from 1.45 ± 0.06 to 2.56 ± 0.35 ml/mln), urine flow (4.82 ± 0.71 to 9.11 ± 1.19 ^il/mln), sodium excretion (0.10 ± 0.02 to 1.15 ± 0.39 M Eq/mln), fractional sodium excretion (0.05% ± 0.02% to 0.43% ± 0.18%), and potassium excretion (0.94 ± 0.08 to 2.50 ± 0.55 /

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mentioning

confidence: 99%

Bilateral renal function responses to converting enzyme inhibitor (SQ 20,881) in two-kidney, one clip Goldblatt hypertensive rats.

Huang¹,

Ploth²,

Bell³

et al. 1981

Hypertension

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“…Kidneys of the one-kidney, one-clip renovascular hypertensive model and the lateral kidneys to the vascular clip in the two-kidney, one-clip renovascular hypertensive model showed similar renal blood flows to the non-restricted kidneys of the hypertensive animals. One study in dogs demonstrates normal renal blood flow and vascular resistances of the contralateral kidney to renal artery stenosis (Zimmerman, Mommsen & Kraft, 1980). However, in the above experiments renal blood flow has been calculated for the whole kidney and not per weight unit, as in the present study and that of Ploth, Roy, Wann-Chu & Navar (1981), where renal blood flow has been found to be decreased.…”

Section: Discussionmentioning

confidence: 50%

Renal Haemodynamics in Conscious Experimentally Hypertensive Rats

Charocopos

1983

Exp Physiol

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SUMMARYThe integrity of renal haemodynamics is essential for the maintenance of normal renal function in the normotensive and hypertensive state. Systemic and renal haemodynamics have been determined by the radioactively labelled microspheres technique in normotensive, Goldblatt I, Goldblatt II and deoxycorticosterone (DOC)-saline-treated hypertensive rats. Cardiac output was similar between normotensive and hypertensive rats, while total peripheral resistance was similarly higher in all hypertensive animals when compared to normotensive animals. Renal blood flow per weight unit was similarly decreased in all hypertensive animals (3 77 ml/min . g (S.D. 0-85, n = I 1); the unclipped kidneys of Goldblatt II rats, 3 76 ml/min . g (S.D. 0 89, n = I 1); the clipped kidneys of Goldblatt II rats, 3 62 ml/min. g (S.D. 078, n = 9); the kidneys of Goldblatt I rats and 2 95 ml/min . g (S.D. 0 83, n = 10) the kidneys of DOC-saline rats). It is concluded that kidneys from experimentally hypertensive rats fail to preserve normal renal blood flow, even at elevated arterial blood pressures, regardless of the pathophysiology of hypertension.

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“…9 In that study, however, guanethidine did not affect the blood pressure of the normotensive controls. Differences in the schedule of drug administration or the agents utilized in the present and previous studies may account for this difference in results.…”

Section: Renal Vasoconstrictor Responses To Phenylephrine B-ht 933mentioning

confidence: 70%

“…We utilized twokidney, one clip Goldblatt hypertensive dogs after the peak in PRA had waned, at which time we presumed they had increased sympathetic tone. 9 Antihypertensive agents that decrease renal vascular resistance, particularly when this is a long-term effect, would be efficacious in the treatment of hypertension. We compared an equally effective a,-receptor blocking dose of urapidil with the more well-characterized blockers, prazosin and phentolamine.…”

Section: Resultsmentioning

confidence: 99%

“…Alternatively, this group of hypertensive dogs may have had a negligible increase in sympathetic tone compared to those observed in our previous study. 9 Urapidil appears to be similar in its peripheral areceptor blocking action to prazosin, because, like prazosin, it blocks a ; -adrenergic receptor sites in the kidney. The ability of these agents to lower renal vascular resistance is attributable in part to an autoregulatory response to the fall in blood pressures.…”

Section: Renal Vasoconstrictor Responses To Phenylephrine B-ht 933mentioning

confidence: 99%

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Relationship of alpha receptor types to hypotension and renal vasodilation caused by alpha blockers in conscious dogs.

Zimmerman¹,

Largent²

1983

Hypertension

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SUMMARY In conscious instrumented normotensive and two-kidney, one clip Goldblatt hypertensive dogs, we compared the effects of the a-receptor blocking agent, urapidil, on blood pressure, renal vascular resistance, heart rate,'and plasma renin activity with those of prazosin and phentolamine. Urapidil (2 mg/kg) and prazosin (0.25 mg/kg) decreased blood pressure and renal vascular resistance in both groups of animals, and urapidil caused a small increase in renal blood flow. Heart rate, but not plasma renin activity, was increased at the peak of the hypotension. Phentolamine had no significant effect on any of these parameters. All three agents markedly inhibited the renal vasoconstrictor responses to intraarterially administered phenylephrine and norepinephrine, and thus exhibited an (*|-receptor blocking action. Only urapidil significantly antagonized the response to B-HT 933, a selective os-receptor agonist, indicating that it also interacts at a 2 -receptor sites. Since both normotensive and hypertensive animals exhibited similar hypotensive responses after both urapidil and prazosin, the degree of a-receptor blockade achieved did not reveal greater sympathetic tone in renal hypertension. VIDENCE suggests that a,-receptors are concentrated at the adrenergic neuroeffector junction, and therefore deblocking agents are particularly effective in inhibiting sympathetic vascular tone.1 Adrenergic blocking agents such as prazosin act selectively on a,-receptors, inhibiting almost completely the vasoconstrictor action of the a,-agonist phenylephrine.2 Agents such as phentolamine, which block both a,-and a,-receptors, have complex effects since they can inhibit sympathetic vascular tone postjunctionally, but also enhance adrenergic transmitter release through blockade of a,-mediated negative feedback.1 Urapidil, a phenyl piperazine derivative, 4 possesses alpha,-blocking properties and may also stimulate a 2 -receptors in the central nervous system.' Thus, this agent has the potential capacity to inhibit sympathetic vascular tone at central and peripheral sites. The main purpose of the present investigation was to examine the effects of urapidil on blood pressure and renal hemodynamics in conscious instrumented normotensive and two-kidney, one clip Goldblatt hypertensive dogs and to ascertain the renal a-adrenergic receptor upon which it acts. MethodsTwelve dogs of either sex weighing 16-30 kg were used in this investigation. Throughout the study, dogs were fed puppy chow, which provided 67 mEq of sodium chloride daily. While anesthetized with pentobarbital, the dogs underwent two separate operations for implantation of femoral arterial and venous catheters, and approximately 1-2 weeks later for placement of a Zepeda blood flow probe (4-5 mm in diameter) around the left renal artery and a PE 10 catheter in the artery. Details of this technique have been published elsewhere. 6 The flow probe was located on the artery as close to the aorta as possible, and the catheter inserted retrograde into the artery at the site of...

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Sympathetic and renin-angiotensin system influence on blood pressure and renal blood flow of two-kidney, one clip Goldblatt hypertensive dog.

Cited by 25 publications

References 33 publications

Bilateral renal function responses to converting enzyme inhibitor (SQ 20,881) in two-kidney, one clip Goldblatt hypertensive rats.

Bilateral renal function responses to converting enzyme inhibitor (SQ 20,881) in two-kidney, one clip Goldblatt hypertensive rats.

Renal Haemodynamics in Conscious Experimentally Hypertensive Rats

Relationship of alpha receptor types to hypotension and renal vasodilation caused by alpha blockers in conscious dogs.

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