Impaired renorenal reflexes in two-kidney, one clip hypertensive rats

In normotensive rats, stimulation of renal mechanoreceptors by an increase in ureteral pressure results in a contralateral inhibitory renorenal reflex response with contralateral natriuresis. Similar effects are produced by stimulation of renal chemoreceptors by renal pelvic perfusion with 0.9 M NaCl. However, in spontaneously hypertensive rats the renorenal reflex responses to renal mechanoreceptor and chemoreceptor stimulation are impaired. The present study was performed to examine whether the renorenal reflexes were altered in two-kidney, one clip hypertensive rats, a model of hypertension in which it has been suggested that the afferent renal nerves contribute to the enhanced peripheral sympathetic nervous activity. A 0.2 mm silver clip was placed around one renal artery 4 weeks before the study. At the time of study, mean arterial pressure was 156 +/- 4 mm Hg. Renal mechanoreceptor and chemoreceptor stimulation of either the nonclipped or clipped kidney failed to affect ipsilateral afferent renal nerve activity, contralateral efferent renal nerve activity, and contralateral urine flow rate and urinary sodium excretion. Renal denervation of the nonclipped kidney increased ipsilateral urinary sodium excretion from 0.65 +/- 0.13 to 1.50 +/- 0.42 mumol/min/g and decreased contralateral urinary sodium excretion from 0.18 +/- 0.03 to 0.13 +/- 0.03 mumol/min/g (p less than 0.05). Thus, denervation of the nonclipped kidney resulted in a similar contralateral excitatory renorenal reflex response as in normotensive rats. However, denervation of the clipped kidney increased both ipsilateral and contralateral urinary sodium excretion, from 0.14 +/- 0.04 to 0.27 +/- 0.5 mumol/min/g and from 1.29 +/- 0.33 to 2.09 +/- 0.59 mumol/min/g (p less than 0.01), respectively. Taken together these data suggest that the lack of inhibitory renorenal reflexes from the clipped kidney may enhance efferent sympathetic nervous activity and thereby contribute to the hypertension in two-kidney, one clip hypertensive rats.     

Vascular renin-angiotensin system in two-kidney, one clip hypertensive rats

The possible role of the renin-angiotensin system in the maintenance of hypertension in two-kidney, one clip hypertensive rats was studied. Plasma renin activity rose rapidly and markedly in association with the elevation of blood pressure and then decreased gradually, although blood pressure remained high. Renin activity in the lung, aorta, and mesenteric artery also increased with the development of hypertension and then decreased in a way similar to that of plasma renin activity at the chronic stage of hypertension. Plasma angiotensin converting enzyme activity did not change significantly until 16 weeks after unilateral renal artery clipping, whereas vascular angiotensin converting enzyme activity significantly increased at the chronic, but not the acute, stage of hypertension. In chronically renal hypertensive rats, 1-sarcosine, 8-isoleucine angiotensin II or enalapril, an angiotensin converting enzyme inhibitor, lowered the blood pressure and enalapril also lowered the angiotensin converting enzyme activity of vascular tissues. The constrictor effect of angiotensin I was greater in isolated arteries from chronically hypertensive rats than in those from age-matched normotensive rats. These results suggest that the vascular renin-angiotensin system plays an important role in the maintenance of two-kidney, one clip hypertension. Elevated vascular angiotensin converting enzyme activity appears to increase local production of angiotensin II, which results in vasoconstriction by acting directly and indirectly through adrenergic nerves on vascular smooth muscle.     

Sodium transport kinetics in erythrocytes from spontaneously hypertensive rats

Rat erythrocytes with five different amounts of Na+ content have been prepared by using a new, nondetrimental Na+-loading method (net NaHPO4-influx through the anion carrier). This method allowed the determination of 1) maximal translocation rates and apparent dissociation constants for internal Na+ of the Na+-K+ pump, outward Na+-K+ cotransport, and Na+-Li+ countertransport and 2) rate constants of Na+ leak in erythrocytes from spontaneously hypertensive rats of the Okamoto strain and Wistar-Kyoto normotensive controls aged 2 to 26 weeks. Two major abnormalities were found in erythrocytes from spontaneously hypertensive rats: 1) a decreased cotransport affinity for internal Na+, which was constantly observed from 2 to 26 weeks of age (mean intracellular Na+ content for half-maximal stimulation of outward Na+-K+ cotransport = 33.1 +/- 7.0 [SD] mmol/L cells in spontaneously hypertensive rats vs 16.7 +/- 4.7 mmol/L cells in Wistar-Kyoto rats; p less than 0.001), and 2) a decreased maximal pump rate in adult (15- to 26-week-old) spontaneously hypertensive as compared with that for age-matched Wistar-Kyoto rats (9-37 vs 34-70 mmol/L cells/hr). Therefore, the low cotransport affinity for internal Na+ appears to be a stable, possibly genetic defect of spontaneously hypertensive rats. Conversely, the decreased maximal pump rate may be a secondary event, possibly reflecting the appearance of endogenous pump inhibitors in the plasma of adult spontaneously hypertensive rats.     

Angiotensin and angiotensin converting enzyme tissue levels in two-kidney, one clip hypertensive rats.

Renal tissue angiotensin I (Ang I) and II (Ang II) content and angiotensin converting enzyme activity were assessed in both kidneys during initial (7 days) and maintenance (25 days) phases of two-kidney, one clip hypertension in rats. At 7 and 25 days, systolic arterial pressure was 146 +/- 2 and 170 +/- 7 mm Hg, respectively. After 7 days, Ang I content of clipped kidneys was 64% and 70% higher (p < 0.001) than in nonclipped and sham-operated kidneys, respectively, when compared with levels in kidneys from sham-operated rats. In kidneys harvested 25 days after clipping one renal artery, Ang I and Ang II contents in clipped kidneys were increased 102% and 24% (p < 0.01), respectively. Ang II content was also 32% higher in nonclipped kidneys. Angiotensin converting enzyme activity in nonclipped kidneys was greater (p < 0.05) than that in either clipped (46% higher) or sham-operated kidneys (57% higher). Plasma Ang I and Ang II levels were elevated at 7 days but were not different at 25 days in clipped rats. These results demonstrate a dissociation between intrarenal and circulating levels of Ang I and Ang II and suggest that qualitatively different mechanisms may be responsible for the elevated intrarenal Ang II levels during the initial and maintenance phases of renal hypertension.     

Effects of angiotensin inhibition and renal denervation in two-kidney, one clip hypertensive rats

Neural and angiotensin-mediated influences that alter hemodynamic and excretory behavior of the nonclipped kidney of two-kidney, one clip hypertensive rats were assessed by sequential acute surgical denervation of the nonclipped kidney and intravenous infusion of converting enzyme inhibitor (SQ 20881), 3 mg/kg X hr. Normal and two-kidney, one clip hypertensive rats (0.2-mm silver clip on the right renal artery 3-4 weeks before study) were prepared to allow study of each kidney. Mean arterial blood pressure of two-kidney, one clip hypertensive rats fell significantly from control values of 149 +/- 6 to 135 +/- 6 mm Hg after denervation of the nonclipped kidney. Despite this decrease in arterial pressure, the nonclipped kidney exhibited significant increases in glomerular filtration rate (from 1.00 +/- 0.08 to 1.24 +/- 0.08 ml/min), sodium excretion (from 88 +/- 39 to 777 +/- 207 nEq/min), fractional sodium excretion (from 0.06 +/- 0.02 to 0.54 +/- 0.14%), and urine flow rate (from 3.7 +/- 0.5 to 8.2 +/- 1.1 microliter/min). A significant decrease in glomerular filtration rate (from 1.12 +/- 0.07 to 0.85 +/- 0.08 ml/min) with no change in excretory function was observed for the clipped kidney following denervation of the nonclipped kidney. Intravenous addition of converting enzyme inhibitor significantly increased renal blood flow (from 7.0 +/- 1.3 to 10.6 +/- 1.5 ml/min) and sodium excretion (from 777 +/- 207 to 1384 +/- 425 nEq/min) for the nonclipped kidney; blood pressure decreased from 135 +/- 6 to 123 +/- 4 mm Hg, and renal vascular resistance decreased significantly (from 22 +/- 3 to 13 +/- 2 mm Hg X min/ml).(ABSTRACT TRUNCATED AT 250 WORDS)     

Vascular neuroeffector function in two-kidney, one clip hypertensive dogs

In control dogs and those made hypertensive for 1 and 8 months by partially occluding a renal artery, contractile responses of mesenteric artery strips to adrenergic nerve stimulation and to norepinephrine, plasma renin activity and vascular angiotensin converting enzyme (ACE) activity were compared. Contractile responses to norepinephrine were potentiated in the artery strips from 8-month-hypertensive dogs; however, the response to electrical stimulation of adrenergic nerves was not influenced. Contractions induced by the nerve stimulation were potentiated by a low concentration (2 X 10(-10) mol/l) of angiotensin (ANG) II; the potentiating effect was enhanced in 8-month-hypertensive dog arteries. 3H-overflow evoked by adrenergic nerve stimulation was increased by ANG II to a greater extent in superfused mesenteric artery strips obtained from hypertensive (8-month) dogs, previously soaked in 3H-norepinephrine. Angiotensin converting enzyme activity was markedly greater in 8-month-hypertensive dog mesenteric arteries than in normotensive dog arteries. It may be concluded that the hypertension is maintained by increased sensitivity of post-synaptic alpha 1-adrenoceptors and pre-synaptic ANG receptors and increased vascular ACE activity, possibly promoting the production of ANG II in the vascular wall.     

Distributions of microvascular pressure in skeletal muscle of one-kidney, one clip, two-kidney, one clip, and deoxycorticosterone-salt hypertensive rats

Studies were performed on the cremaster skeletal muscle in rats to investigate the microvascular changes that are associated with established one-kidney, one clip (1K1C) and two-kidney, one clip (2K1C) Goldblatt hypertension and with deoxycorticosterone (DOC)-salt hypertension. Rats were anesthetized with urethane and chloralose; and cremaster muscles with intact circulation and innervation were suspended in a controlled Krebs bath. Microvascular pressures and vessel diameters were measured at three consecutive arteriolar (A) and venular (V) branch levels. Arteriolar diameters (means +/- SEM) in normotensive (NT) rats were 119 +/- 7, 86 +/- 5, and 31 +/- 3 micron respectively for 1A, 2A, and 3A arterioles; and venule diameters were 218 +/- 12, 141 +/- 15, and 53 +/- 7 micron respectively for 1V, 2V, and 3V venules. As compared to NT rats, there was a selective decrease in lumen size (percent reduction from control) for 1A and 2A (23% to 38%) in 1K1C and 2K1C rats and for 1A, 2A, and 3A (42% to 44%) in DOC rats. Venule diameters were not significantly different between normotensive and hypertensive animals at any branch level. Femoral artery pressures were significantly elevated (greater than or equal to 43%) in all three forms of hypertension; however, this increase in pressure was not proportionally transmitted throughout the microcirculation. This was evidenced by normal pressure in 3A arterioles and in all venules for 1K1C and 2K1C rats and by normal pressures in 3V and larger venules for DOC rats. Our findings indicate that elevated arterial pressure in chronic renal hypertension is not transmitted uniformly across all microvascular segments.(ABSTRACT TRUNCATED AT 250 WORDS)     

Unclipping of two-kidney, one clip hypertensive rats produces endothelium-dependent inhibition of sympathetic vasoconstriction

Removal of the renal artery-constricting clip in two-kidney, one clip (2-K,1C) Goldblatt-hypertensive rats produces a rapid fall in blood pressure which has been attributed to the release of vasodepressor lipids from the renal medulla. The aim of this study was to demonstrate the effect of unclipping 2-K,1C hypertensive rats, and of any hormone thereby released, on vasoconstrictor responses to sympathetic stimulation in the ex vivo blood-perfused tail artery, as well as the role of the vascular endothelium in mediating this effect. Blood was withdrawn at a rate of 2 ml/min from the carotid artery of an anaesthetized 2-K,1C rat and used to perfuse, via an extracorporeal circuit, a cannulated segment of tail artery which had been taken from a killed, normal rat and mounted in an organ bath. The blood was returned to the 2-K,1C rat via the jugular vein. Vasoconstriction and increases in perfusion pressure were produced by periarterial electrical stimulation of the tail artery. The tail artery was either intact or had had its endothelium removed. Sham operations which did not remove the renal artery clip did not change blood pressure or vasoconstrictor responses. Unclipping lowered blood pressure and reduced vasoconstrictor responses in ex vivo blood-perfused tail arteries in which the endothelium was intact, but did not decrease responses in tail arteries from which the endothelium had been removed. It is concluded that unclipping releases a hormone which lowers blood pressure and inhibits sympathetic vasoconstrictor responses via an endothelium-dependent mechanism.     

In vivo left ventricular anatomy in rats with two-kidney, one clip and one-kidney, one clip renovascular hypertension.

OBJECTIVES: To evaluate differences in left ventricular structural changes related to different hemodynamic patterns. DESIGN: One-kidney, one clip (1K1C; volume-dependent hypertension) rats were two-kidney, one clip (2K1C; high-resistance hypertension) to determine whether these two types of Goldblatt rats showed different types of left ventricular adaptation. METHODS: M-mode echocardiography was used to study 28 2K1C and 19 1K1C Wistar rats 8 weeks after surgery and 55 age-matched control animals. RESULTS: Systolic blood pressure was equally high in the two models; the 1K1C rats had a larger left ventricular chamber and normal plasma renin activity (PRA), whereas in the 2K1C rats PRA was increased and the left ventricular chamber was normal. The atrial natriuretic factor was significantly increased only in the 2K1C rats and was related to PRA. The left ventricular mass index was increased in both models, but more in the 1K1C than the 2K1C rats. CONCLUSIONS: In both models the degree of left ventricular hypertrophy was associated with the interacting effects of the hemodynamic component superimposed on the primary hemodynamic pattern (i.e. blood pressure as an expression of pressure overload in the primarily volume-dependent 1K1C rats and the left ventricular chamber size as an expression of volume overload in the high-resistance 2K1C rats). The interaction between pressure and volume increased the left ventricular wall thickness in both models, with additional chamber enlargement in the 1K1C rats. In these rats, the increase in left ventricular mass was more pronounced due to the greater volume load on the heart.     

Effect of DOCA-salt on angiotensin dependency and surgical reversal of hypertension in two-kidney, one clip renal hypertensive rats

The development of hypertension in two-kidney, one clip renal hypertensive rats (2K, 1C RHR) was not altered by treatment with DOCA and saline solution as drinking fluid for two months of observation. However, the administration of DOCA and salt suppressed plasma renin activity (PRA), the renal renin content (RRC) of the clipped kidney and the response to a single oral dose of captopril (10 mg/kg). The weight of the contralateral kidney was increased by the administration of DOCA-salt, while that of the ischaemic kidney was not changed. The withdrawal of DOCA-salt treatment restored the PRA and the effects of captopril to a similar degree to the non-treated group. The acute hypotensive effects of captopril were reduced on the 10th week compared with the 7th week after renal arterial constriction in 2K, 1C RHR. The fall in blood pressure induced by captopril significantly correlated with the initial PRA both in the 7th and 10th week after clipping. There was a significant correlation between PRA and RRC of the clipped kidney. Rats previously treated with DOC-salt had either removal of the contralateral kidney with removal of the clip from the ischaemic kidney, or removal of the ischaemic kidney. Blood pressure fell to normal levels in the unclipped group and in the nephrectomy group, but the fall in the latter group was transient and within two weeks had risen to significantly higher levels than in the unclipped group. It is concluded that structural vascular change following DOC-salt hypertension is insufficient to cause persisting hypertension except when it occurs in the renal circulation.     

Arterial pressure and renal function in two-kidney, one clip Goldblatt hypertensive rats maintained on a high-salt intake

Arterial blood pressure and renal function of both clipped and non-clipped kidneys of benign two-kidney, one clip (2K1C) Goldblatt hypertension were evaluated in order to determine whether high-salt intake alters the course of the development and magnitude of hypertension or influences renal function. The administration of 0.9% sodium chloride as a drinking solution for 3 weeks suppressed plasma renin activity (PRA) and kidney renin content of the clipped kidney to normal values. Despite suppression of PRA and kidney renin content, the saline-drinking clipped rats still developed hypertension of the same magnitude as the water-drinking clipped rats. However, the onset of hypertension was delayed by 4 days. Urine flow, glomerular filtration rate (GFR) and sodium excretion rate from the clipped kidneys of the saline-drinking clipped rats were higher than the corresponding values in the water-drinking rats, and approached those observed in control animals. Thus, the high-salt intake which was associated with suppression of the activity of the renin-angiotensin system delayed the onset of, but not the final magnitude of, the hypertension. In addition, kidney function in the clipped kidneys of saline-drinking clipped rats was enhanced compared with that observed in the water-drinking clipped rats.     

A comparison of the actions of cilazapril in normal, dietary sodium-depleted and two-kidney, one clip Goldblatt hypertensive anaesthetised rats.

OBJECTIVE: This study aimed to examine the role of the renin-angiotensin system in the regulation of kidney haemodynamic and excretory function when angiotensin II levels were modestly and markedly raised. DESIGN: Three groups of male Sprague-Dawley rats were used: control rats fed a sodium-replete diet; rats fed a sodium-deficient diet for 2 weeks; and two-kidney, one clip (2K1C) Goldblatt hypertensive rats, 4-5 weeks postclipping. METHODS: The rats were acutely anaesthetized with sodium pentobarbitone and prepared for renal function measurements. The converting enzyme inhibitor, cilazapril, was then infused at increasing dose levels to progressively block the renin-angiotensin system. RESULTS: Cilazapril did not affect blood pressure in sodium-replete animals; it raised RBF and increased water and sodium excretion. In dietary sodium-depleted rats, cilazapril decreased blood pressure and increased RBF, water and sodium excretion at the lower doses of the drug; however, at vasodepressor doses, water and sodium excretion fell towards baseline values. In 2K1C Goldblatt hypertensive rats, cilazapril maximally decreased blood pressure whilst the non-clipped kidney blood flow, filtration rate and fluid excretion rates were similar to dietary sodium-depleted rats; in contrast, the clipped kidney filtration rate was well maintained and fluid excretion was raised in a dose-related fashion. CONCLUSION: These results show that during gradual cilazapril administration, renal function is well preserved in 2K1C Goldblatt hypertensive rats when pressure is progressively reduced.     

Changes of plasma renin activity following intracerebroventricular administration of biologically active peptides in two-kidney, one clip hypertensive rats

We studied the effects of intracerebroventricular (ICV) administration of angiotensin II (ANG II), bradykinin (BK), leucine-enkephalin (Leu-ENK) and neurotensin (NT) on plasma renin activity (PRA), blood pressure and heart rate in acute (less than 4 weeks) and chronic (more than 12 weeks) two-kidney, one clip (2K-1C) hypertensive rats. These four peptides all produced pressor responses. The pressor responses caused by ICV injection of ANG II, BK, Leu-ENK and NT in hypertensive rats did not differ significantly from the response in normal rats. In both acute and chronic 2K-1C hypertensive rats, ANG II and BK significantly suppressed PRA, NT did not affect PRA, and Leu-ENK produced a significant increase in PRA followed by a significant decrease in PRA. As compared to normal rats, suppression of PRA by ANG II and NT was attenuated or abolished but BK and Leu-ENK produced significant reductions in PRA in 2K-1C hypertensive rats. The results indicate that the effects of these four centrally administered peptides on blood pressure, heart rate and PRA in acute and chronic 2K-1C hypertensive rats were not essentially different from those in normal rats.     

Vascular and cardiac overexpression of endothelin-1 gene in one-kidney,one clip Goldblatt hypertensive rats but only in the late phase of two-kidney one clip Goldblatt hypertension

OBJECTIVE: To investigate a model of experimental hypertension that exhibits severe hypertrophy of small blood vessels but in which deoxycorticosterone acetate (DOCA) and salt are absent: the one-kidney, one clip model of Goldblatt renovascular hypertension, which is non-renin-dependent, and compare it with the renin-dependent two-kidney, one clip Goldblatt hypertensive rat, in which additionally vascular hypertrophy is less severe. METHODS: Endothelin-1 gene expression in blood vessels and in the heart was examined by Northern blot analysis. RESULTS: After 2 or 4 weeks of application of the silver clip to unilaterally nephrectomized rats, the aorta and mesenteric arteries exhibited a significant increase in the intensity of the 2.3 kb band corresponding to hybridization with endothelin-1 messenger RNA (mRNA) in comparison with results obtained in control unilaterally nephrectomized rats. No increase was noted in the blood vessels of the two-kidney, one clip hypertensive rat at 2 or 4 weeks, but significant increases were found at 8 weeks in aorta, but not in mesenteric arteries. Cardiac abundance of endothelin-1 mRNA was also increased in ventricles and in the left atria of one-kidney, one clip hypertensive rats, but only in the late phase (at 8 weeks) in two-kidney, one clip hypertensive rats. CONCLUSION: Because one-kidney, one clip hypertensive rats presented severe vascular hypertrophy whereas two-kidney, one clip hypertensive rats only did so in the late phase of hypertension, these results lend further support to there being a relationship between vascular hypertrophy and endothelin-1 vascular overexpression in experimental models of hypertension. They also demonstrate that enhancement of the expression of endothelin-1 gene in blood vessels and in the heart of hypertensive rats may occur in the absence of exposure to DOCA and salt, and that endothelin-1 gene overexpression in experimental hypertension occurs early in non-renin-dependent, volume-expanded models such as the one-kidney, one clip or the DOCA-salt hypertensive rat, but only in the progressively non-renin-dependent late phase of the initially renin-dependent volume-contracted two-kidney, one clip hypertensive rat.     

Sympathomedullary activity in one-kidney, one clip hypertensive rats

In order to evaluate more directly the implications of the sympatho-adrenal system in one-kidney, one clip hypertension (1K1C), we studied adrenal catecholamine synthesis after a bolus injection of 3H-tyrosine, tissue norepinephrine and dopamine concentrations, as well as the urinary excretions of norepinephrine, epinephrine, dopamine and those of the major dopamine metabolites, dihydroxphenylacetic acid (DOPAC) and homovanillic acid (HVA) in 1K1C and control uninephrectomized rats. When compared with controls, the hypertensive rats had a markedly enhanced formation of adrenal 3H-norepinephrine and 3H-epinephrine, higher urinary norepinephrine and epinephrine excretions but lower heart and kidney content of norepinephrine and dopamine as well as decreased urinary excretions of the main dopamine metabolites, DOPAC and HVA. These data suggest an increased norepinephrine and epinephrine synthesis in 1K1C hypertensive rats associated with dopamine synthesis, which is normal but probably disproportionally low relative to the synthesis of norepinephrine and epinephrine. This abnormality may be an important pathogenetic factor in this model of experimental hypertension.     

Chronic captopril infusion in two-kidney, one clip rats with normal plasma renin concentration

Immediately after clipping, plasma renin and angiotensin II concentrations are raised in the two-kidney, one clip rat. Plasma renin and angiotensin II fall to relatively low levels between two and five weeks after operation, while blood pressure continues to rise. An experiment was carried out to determine whether complete suppression of angiotensin II during this two- to five-week period would have any effect on the development of hypertension. Captopril infused chronically (2 mg/kg/h) for up to 20 days completely prevented the rise in mean blood pressure [110.8 +/- 17.9 at day 0 compared to 88.3 +/- 8.4 (s.d.) mmHg at day 20] seen in an equivalent control group infused with dextrose (109.2 +/- 11.6 at day 0 compared to 131.7 +/- 23.6 mmHg at day 20). Preinfusion values for plasma renin and angiotensin II concentration were within the upper half of the range found for sham-operated normal rats. These findings would suggest that while the plasma levels of angiotensin II are low in relation to those seen immediately after clipping, they are still raised in comparison with normal sham-operated rats; this may contribute to the development of hypertension by a slow chronic, rather than an acute, effect.     

Renal atrial peptide receptors and natriuresis in two-kidney, one clip hypertension.

It has been suggested that the impaired natriuretic response of the clipped kidney in two-kidney, one clip hypertensive rats is related to downregulation of renal atrial natriuretic peptide receptors. To test this hypothesis, blood volume expansion and atrial peptide binding studies were performed in this model. Infusion of 1% and then 1.5% body weight donor blood (n = 6) caused a progressive increase in plasma immunoreactive atrial natriuretic peptide (107 +/- 26 to 168 +/- 31 to 427 +/- 154 pg/ml, p less than 0.001); the sodium excretion of the nonclipped kidney rose from 230 to 2,200 to 4,000 neq/min (p less than 0.01) but that of the clipped kidney did not rise significantly. There was a highly significant correlation between log cyclic guanosine monophosphate and log sodium excretion by the nonclipped (r2 = 0.749) but not the clipped (r2 = 0.046) kidney. Between clipped and nonclipped kidneys, the association constant (5.26 +/- 0.89 versus 5.17 +/- 0.64 x 10(9)/mol) and apparent binding site density (575 +/- 92 versus 500 +/- 74 fmol/mg protein) for atrial peptide binding in isolated glomeruli did not differ. Assay of atrial peptide-induced cyclic guanosine monophosphate release by isolated glomeruli showed that clipped and nonclipped kidneys were equally responsive. Binding affinity and receptor density did not differ in homogenates prepared from inner medullas of clipped and nonclipped kidneys. These results show that the blunted natriuretic response in clipped kidneys was not associated with any relative decrease in number or function of glomerular or papillary atrial natriuretic peptide receptors.