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Biomedical subjects

T A Kotchen

Publications and source records attributed to T A Kotchen.

At least 145 records · Page 8Linked to original sources
PubMed1977

Renin and aldosterone in the cardiomyopathic hamster in congestive heart failure.

The renin-aldosterone system was studied in cardiomyopathic hamsters (CMH) before and after the onset of untreated clinical congestive heart failure. Age-matched random-bred hamsters (RB) served as controls. Before heart failure, there were no differences in body weight accretion, sodium balance, plasma renin activity or in vitro aldosterone production. After the onset of heart failure in CMH, body weight increased at a greater rate than in RB and positive sodium balance was nearly twice control levels. Although plasma renin activity was greater (P less than 0.005) in CMH than in RB (23.4+/-4.2 (mean+/-SEM) vs. 3.8+/-1.8 ng/ml/h), aldosterone production (101+/-15 vs. 95+/-16 ng/h) did not differ. Plasma aldosterone was low or undetectable in RB and in CMH in heart failure. In response to angiotensin stimulation, aldosterone production increased in both strains and did not differ. No difference in muscle potassium content, potassium balance or excretion was detected. Thus, in CMH, congestive heart failure is attended by increased plasma renin activity without a significant increase in aldosterone production, a dissociation which does not appear to be due to adrenal unresponsiveness to angiotensin II or to potassium depletion.

Adrenal Glands↗
PubMed1977

Renin reactivity in plasma of patients with normal renin and low renin essential hypertension.

Plasma renin reactivity (PRR) is the rate of angiotensin generation in vitro after addition of exogenous renin to plasma. To evaluate the hypothesis that suppressed plasma renin activity (PRA) in patients with low renin essential hypertension may be related to an alteration of the kinetics of the in vitro renin reaction, PRR was compared in plasma of patients with low renin and normal renin essential hypertension. Prostaglandin A (PGA) inhibits renin, and PGA was also measured to determine if suppressed PRA may be related to increased PGA. Low renin and normal renin hypertension were defined by comparing PRA responses of 30 hypertensive patients and 16 matched control subjects to upright posture and furosemide (80 mg p.o.). Nine of 30 patients had low PRA. Compared to that in plasma of patients with normal renin hypertension, PRR was suppressed (P less than 0.005) during 30, 60, and 180 min incubations in the low renin patients. Overall, in the hypertensive patients, there was a significant positive correlation (r= +0.58; P less than 0.01) between PRR and the PRA response to furosemide. PGA in patients with low renin hypertension (0.86 ng/ml+/-0.06 SE) was less (P less than 0.05) than that in patients with normal renin hypertension (1.10 ng/ml+/-0.07) SE) and control subjects (1.18 ng/ml+/-0.10 SE); PGA of normal renin patients and control subjects did not differ (P less than 0.1). These results suggest that an alteration of the kinetics of the renin reaction may contribute to the apparent renin suppression in patients with low renin hypertension. Hypertensive patients with suppressed PRA also have low PGA.

Carbon Dioxide↗
PubMed1977

Effect of calcium gluconate infusion on renin in the dog.

We have previously reported that infusion of CaCl2 into the renal artery of the dog inhibits renin release. To evaluate the possible importance of the anion delivered with calcium, similar experiments were performed in 10 dogs with equivalent amounts of calcium gluconate (0.3 mg. of Ca++ per kilogram of body weight per minute). The experiment consisted of three successive 15 minute control periods, followed by three 15 minute calcium gluconate infusion periods and two 15 minute recovery periods. During calcium gluconate infusion, mean serum Ca++, and ECa++, ENa+, and EFNa+ from the infuses kidney increased (p less than 0.005). Systolic blood pressure (142 mm. Hg +/- 8S.E.), renal blood flow (137 ml. per minute +/- 11 S.E.), creatinine clearance, and aldosterone excretion (12.0 ng. per 15 minute +/- 1.5 S.E.) did not change (p less than 0.3). Renal venous PRA (28.4 ng. per millileter per hour +/- 7.5 S.E.) decreased (p less than 0.014). The per cent decrease of PRA correlated (r = -0.70) with the per cent increase EFNa+ (p less than 0.001). Calcium gluconate had a lesser (p less than 0.01) inhibitory effect on renin than CaCl2, despite greater excretion of Ca++ and Na++ during calcium gluconate infusion. Taken together, the results indicate that Ca++ inhibits renin release, although the extent of the inhibition is modified by the anion accompanying Ca++. The effect of Ca++ on renin may be mediated by NaCl transport across the macula densa.

Animals↗
PubMed1976

Failure of NaHCO3 and KHCO3 to inhibit renin in the rat.

To evaluate the contribution of chloride to NaCl- and KCl-induced renin inhibition, renin responses to NaCl or NaHCO3 and to KCl or KHCO3 loading were compared in NaCl-deprived rats. Sodium balance in animals drinking isotonic NaHCO3 and NaCl for 9 days did not differ (P greater than 0.40); K+ balance was less positive in NaHCO3-drinking animals (P less than 0.005). Plasma renin activity (PRA) in NaCl-loaded (16.5 ng/ml per h +/- 4.4 SE), but not in NaHCO3-loaded rats (57.2 +/- 9.8), was lower (P less than 0.005) than in NaCl-deprived controls (44.8 +/- 4.7). Renal renin content (RRC) of NaCl but not of NaHCO3-drinking animals was also decreased (P less than 0.02). Both PRA and RRC of KCl- but not of KHCO3-loaded rats (5 meq K+/10 g diet) were lower (P less than 0.01) than in NaCl-deprived controls. After acute intravenous expansion with isotonic NaCl or NaHCO3, increases of plasma volume and plasma K+ did not differ (P greater than 0.05). However, PRA of NaCl-expanded rats (11.8 +/- 3.8) was lower (P less than 0.05) than in NaHCO3-expanded animals (29.7 +/- 8.5). The failure of NaHCO3 and KHCO3 to inhibit renin suggests a role for chloride in mediating the renin responses to Na+ and K+.

Acid-Base Equilibrium↗
PubMed1976

Modification of renin reactivity by lipids extracted from normal, hypertensive, and uremic plasma.

Plasma renin reactivity (PRR), the in vitro rate of angiotensin generation after addition of renin, is greater in plasma of hypertensive patients and uremic patients than in plasma of normotensive control subjects. To determine if this difference is due to different substrate reactivities, substrate was denatured and replaced with homologous substrate. After a 180 min incubation, PRR in normal plasma (73 ng/ml +/- 5 SE) was less (P less than 0.01) than that in hypertensive (112 ng/ml +/- 15 SE) or uremic (123 ng/ml +/- 39 SE) plasma. To determine if uremic plasma lacks a renin inhibitor, buffer or plasma was added to renin-renin substrate. Less angiotensin was generated (P less than 0.05) with normal (72 ng/ml +/- 4 SE) and uremic (88 ng/ml +/- 4 SE) plasma during 30 min than with buffer (107 ng/ml +/- 4 SE). After 180 minutes, less angiotensin was generated with normal (P less than 0.05) but not uremic plasma (P greater then 0.6), than with buffer. In vitro angiotensin generation was inhibited by lipids extracted from normal plasma. Lipids were separated into acetone soluble (neutral lipids) and acetone insoluble (phospholipid) fractions. Acetone soluble lipids, extracted from normal plasma, competitively inhibit renin: renin was not inhibited by acetone insoluble lipids. Acetone soluble lipids extracted from uremic plasma inhibited PRR to a lesser extent than lipids from either normal plasma or hypertensive plasma (P less than 0.01). Increased PRR in uremic plasma may be related to the deficiency of a circulating acetone soluble renin inhibiting factor.

Angiotensin II↗
PubMed1976

Hypertension detection and control in a rural white Kentucky community.

This report presents data on the prevalence of elevated blood pressure and the status of hypertension control in a rural Kentucky community. Medical care is provided to the population under study by a long established organization of nurse practitioners. With the exception of young males, detection of hypertension has been relatively successful. However, fewer than 50 per cent of persons with blood pressure greater than 160/100 mmHg are receiving antihypertensive therapy, and greater than 60 per cent of individuals on therapy have blood pressure greater than 160/100 mmHg. Despite detection of hypertension control has not been achieved in this rural white community.

Adolescent↗
PubMed1976

Prevalence of hypertension in a renal transplant population on alternate-day steroid therapy.

A study of the prevalence of hypertension in a group of renal transplant patients on alternate-day maintenance steroid therapy was conducted. Twenty-four percent of the transplant clinic population was hypertensive. The factors that were associated with a lower prevalence of hypertension were good graft function, bilateral nephrectomy of the patients' own diseased kidneys (although the majority of our patients without bilateral nephrectomy are normotensive), and use of a living related donor. We conclude that the prevalance of hypertension in transplant patients on alternate-day steroid therapy is low. In the presence of all these favorable factors, only 6% of allograft recipients were hypertensive.

Adolescent↗
PubMed1976

Detecting and treating arteriosclerotic renovascular hypertension.

Renovascular hypertension is the most prevalent form of surgically remediable hypertension. With appropriate selection of operative candidates, a high rate of cure or improvement may be anticipated. Favorable results justify revascularization in hypertensive patients with focal arteriosclerotic renal artery disease. The absence of advanced arteriosclerosis provides the most valid basis for predicting long-term survival following revascularization. Patients with clinically demonstrable diffuse arteriosclerotic disease are preferably treated medically; we consider them candidates for surgery only if drug therapy cannot control blood pressure. Renal revascularization does not appear to alter the inexorable progression of concomitant generalized arteriosclerosis. Revascularization rather than nephrectomy is the primary surgical therapy for renal artery stenosis in properly selected patients.

Adolescent↗
PubMed1976

Relationship between collateral development and renin in experimental renal arterial stenosis.

Lateralizing renal venous plasma renin activity (RVPRA) ratios offer a predictive index of success of revascularization procedures for renovascular hypertension. Reliance upon nonlateralizing renin ratios to reject functional significance of renal arterial stenosis may deny some patients benefit of successful operations. To test the hypothesis that RVPRA ratios revert toward unity coincident with development of collateral circulation to an ischemic kidney, the relationship between development of collaterals and RVPRA was studied in nine dogs after gradual unilateral renal arterial occlusion with a constrictor. Arterial blood pressure and arteriographic measurement of collateral channels, RVPRA, and renal surface index (RSI) were measured before and during the 10-week interval after constrictor placement. RSI measurements, documenting changes in volume of the renal parenchyma, reflected changes in renal blood flow. Arterial pressure increased in each animal (p less than 0.0009). The number of collateral vessels to the constricted kidney increased with time (p less than 0.01). During the 4 weeks following placement of the constrictors, RSI ratios (constricted: nonconstricted) decreased (p less than 0.003) and RVPRA ratios (constricted: nonconstricted) increased (p less than 0.005). Subsequently, coincident with development of collateral vessels, RSI ratios increased and RVPRA ratios decreased toward control values. These data suggest that absence of lateralizing RVPRA ratios in the presence of collateral vessels does not mean lack of functional significance of stenotic renal arterial lesions.

Animals↗
PubMed1975

Effect of KCl infusion on renin secretory rates and aldosterone excretion in dogs.

The effects of unilateral intrarenal arterial KCl infusion in dogs (12 mueq/kg per min) on bilateral renal function, renin secretory rates, and aldosterone excretion were studied. During KCl infusion, infused-side renal arterial plasma [K+] increased by 2.2 +/- 0.6 meq/liter. Systemic plasma [K+] simultaneously rose by 0.6 +/- 0.1 meq/liter. Plasma renin activity decreased 29 +/- 9%, and the decrease correlated with the increases in plasma [K+]. Renin secretory rate decreased bilaterally, the decrease being greater in each experiment on the infused side. Aldosterone excretion increased during KCl infusion by 72 +/- 17%, despite a decrease in plasma renin activity. With KCl infusion there was a bilateral increase in K+ excretion, and a positive correlation was observed between the net alterations in K+ and Na+ excretion. No significant alterations in systemic blood pressure, glomerular filtration rate, total renal blood flow, or intracortical renal blood flow distribution were observed. These studies suggest that K+ inhibits the release of renin by an intrarenal mechanism, which may be related to a K+-induced alteration in Na+ absorption.

Aldosterone↗
PubMed1975

Evidence for the existence of an acetone soluble renin inhibiting factor in normal human plasma.

After addition of exogenous human renin, the in vitro rate of angiotensin I generation is faster in plasma of patients with chronic renal insufficiency and, to a lesser extent, in plasma of patients with essential hypertension than in plasma from normotensive control subjects. The increased reactivity of renin in hypertensive and uremic plasma is not related to differences of endogenous renin activity, angiotensinase activity, renin substrate concentration, or substrate reactivity. Addition of normal, hypertensive, and uremic plasma to a human renin-sheep renin substrate system inhibited the rate of angiotensin generation, although significantly less inhibition was observed with uremic plasma. The reactivity of renin increased in normal plasma but not in uremic plasma after treatment with 95% acetone. After acetone extraction renin reactivity in normal and plasma inhibited the rate of angiotensin generation in a renin-renin substrate system. Less inhibition occurred with the acetone extract from a pool of uremic plasma. These results provide evidence for the existence of a naturally occurring acetone soluble renin inhibiting factor in normal and uremic plasma. The increased reactivity of renin in uremic plasma may be related to a deficiency of this factor.

Acetone↗