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Biomedical subjects

T A Kotchen

Publications and source records attributed to T A Kotchen.

At least 109 records · Page 6Linked to original sources
PubMed1982

Blood pressure of young mothers and their children after hypertension in adolescent pregnancy: six- to nine-year follow-up.

To determine if gestational hypertension during adolescent pregnancy is associated with subsequently elevated blood pressure, blood pressures were measured in young mothers 3-6 years and again at 6-9 years after their first pregnancy. Follow-up study groups were selected from an original study population of 409 pregnant adolescent women followed at the university of Kentucky Medical Center between 1971 and 1974 in a specially designated Young Mothers' Program. Blood pressures measured during the first and second follow-up surveys were highly correlated. Compared to matched control subjects who remained normotensive throughout pregnancy (n = 54), women with a history of hypertension during pregnancy (n = 70) were heavier, maintained higher blood pressure, and had a greater incidence of hypertension in subsequent pregnancies. At the second follow-up survey, systolic blood pressure and body weight of male children born to women who experienced gestational hypertension were greater than respective values in males born to women with normotensive pregnancies. Blood pressures of female children of the two groups of young mothers did not differ. Overall, blood pressures and body weights of young mothers correlated with blood pressures and body weights of both their children and their own mothers. The results suggest that gestational hypertension may unmask a tendency for hypertension.

Adolescent↗
PubMed1982

Adrenergic responsiveness in prehypertensive subjects.

To determine if alterations in adrenergic activity precede hypertension, we evaluated the pressor effect of an alpha agonist (phenylephrine) and the chronotropic effect of a beta agonist (isoproterenol) in prehypertensive young men. The subjects were selected from a 5-year follow-up of individuals in the upper ("high") and lower ("low") deciles of the blood pressure distribution in a high school population. At follow-up, the blood pressure differences between groups were maintained. The baroreflex slopes of the high (n = 13) and low (n = 10) blood pressure groups did not differ. The dose of phenylephrine required to increase systolic blood pressure by 20 mm Hg (PD20) was greater in the high blood pressure group than in the low blood pressure group (250 +/- 38 micrograms vs 167 +/- 35 micrograms, p less than 0.05). The dose of isoproterenol required to increase the heart rate by 25 beats/min (CD25) was also greater in the high than in the low blood pressure group (1.9 +/- 0.5 micrograms vs 0.9 +/- 0.2 micrograms, p less than 0.05). The increase in plasma renin activity in response to treadmill exercise was less in the high than in the low blood pressure group (1.8 +/- 0.6 ng/ml/hr vs 3.4 +/- 0.7 ng/ml/hr, p less than 0.03). Overall, systolic blood pressure correlated with PD20 (r = 0.52, p less than 0.01) and CD25 (r = 0.62, p less than 0.001). Plasma norepinephrine correlated with systolic blood pressure (r = 0.44, p less than 0.04) and with PD20 (r = 0.63, p less than 0.001). We conclude that baroreflex sensitivity is not altered in young men with relatively high blood pressure. Insensitivity to alpha and beta agonists may be related to the positive correlation of systolic blood pressure with plasma norepinephrine concentration.

Adolescent↗
PubMed1982

Low renin-aldosterone in "prehypertensive" young adults.

PRA is suppressed in approximately 25% of patients with essential hypertension. To determine if renin suppression precedes the onset of hypertension, PRA and plasma aldosterone were measured before and after treadmill exercise in 129 young adults with relatively high, intermediate, or relatively low blood pressures sustained over 5 yr. PRA and aldosterone responses to exercise were lower (P less than 0.01) in the high blood pressure group. In contrast, plasma renin substrate was lower (P less than 0.01) in the low blood pressure group. Unrelated to blood pressure, PRA, but not aldosterone, was lower in black than in white subjects both before and after exercise. In conclusion, renin suppression precedes the onset of hypertension and may be an appropriate response to higher levels of arterial pressure.

Adolescent↗
PubMed1982

Renin and aldosterone responses to short-term NaCl or NaHCO3 loading in man.

We compared the effects of 500 ml of 0.15M NaCl or 750 ml of 0.15M NaHCO2, infusions on PRA and PAC in 16 normal NaCl-restricted men. More positive sodium balance, greater natriuresis, and lower serum chloride, potassium, and hydrogen ion concentrations were observed after NaHCO3 infusion. PRA decreased (13.8 +/- 1.0 ng/ml angiotensin I per hour to 6.6 +/- 0.70) and PAC did not change (98 +/- 15 ng/dl to 86 +/- 15) after NaCl infusion. Conversely, PRA did not change (9.9 +/- 1.6 to 10.1 +/- 1.6) and PAC decreased (85 +/- 9 to 44 +/- 5) after NaHCO3 infusion. Plasma cortisol declined in both groups. These results suggest that in sodium-restricted man chloride is more important than sodium for the suppression of PRA by NaCl loading and that potassium or hydrogen ion is a more sensitive modulator of aldosterone secretion than is renin.

Adult↗
PubMed1981

Effect of hypochloremia on loop segment chloride and solute reabsorption in the rat during volume expansion.

Hypochloremia has been associated by inference from clearance studies with disturbances in free water reabsorption and renal renin release by a macula densa mechanism. To examine directly these relationships, we studied chloride, fluid, and solute transport in the loop segment (LS) of rat superficial nephrons by micropuncture techniques following acute volume expansion with 0.15 m sodium chloride (CVE) or sodium bicarbonate (BVE). Plasma renin activity was suppressed in group CVE but not in group BVE. Blood pressure, plasma volume expansion, whole kidney GFR, urinary sodium excretion, late proximal and early distal SNGFR, and fluid delivery to the LS were no different between groups CVE and BVE despite different plasma chloride concentrations (102 +/- 5 mEq/liter for CVE vs. 74 +/- 3 for BVE; P less than 0.001). Absolute LS chloride reabsorption was less in BVE than it was in CVE (2030 +/- 120 pEq/min vs. 2454 +/- 136; P less than 0.025). This was associated with significantly lower fractional absolute LS solute reabsorption and higher early distal tubule fluid osmolality. These data demonstrate directly and in vivo that a decrease in chloride reabsorption in the LS of superficial nephrons is associated with impaired solute reabsorption in that segment and a failure to suppress plasma renin activity by sodium loading.

Absorption↗
PubMed1981

Surgical therapy for persistent hypertension after renal transplantation.

The presence of the original diseased native kidneys in renal allograft recipients is associated with an increased prevalence of persisting post-transplant hypertension. In 9 of 10 such transplant patients bilateral nephrectomy of these native kidneys, performed at least 1 year after successful transplantation of a renal allograft, resulted in improved blood pressure control. Although these 10 patients had higher peripheral plasma renin activity (PRA) than normotensive patients (5.9 +/- 1.3 ng/ml/hr versus 1.5 +/- 0.3 mg/ml/hr), selective renal vein renin measurements did not consistently demonstrate higher renin concentrations from the native kidneys. Removal of the original kidneys was beneficial even in some patients who had stenosis of the allograft artery demonstrated by arteriography.

Follow-Up Studies↗
PubMed1981

Increased enzymatic activity of renin and hyperlipidemia.

We have previously reported that the in vitro enzymatic activity of exogenous renin, plasma renin reactivity (PRR), is increased in plasma of patients with chronic renal failure, possibly due to the deficiency of a renin inhibitor. To determine whether increases PRR is related to renal failure per se or to hyperlipidemia, PRR was measured in 10 control subjects, 10 patients with renal failure, and 10 hyperlipidemic patients with normal renal function. Compared to that in control subjects (52.6 ng angiotensin I generated per ml/h +/- 3.8 SE) PRR was increased (P < 0.05) in plasma of uremic patients (65.1 +/- 4.3) and hyperlipidemic patients (71.4 +/- 10.7). Renin substrate concentration did not differ among groups, and after denaturation of endogenous substrate by acidification of plasma, PRR was still increased. A "protein-free" extract of plasma from normal subjects inhibited renin, whereas little or no inhibition occurred with a comparable extract from uremic patients and hyperlipidemic patients. Thus, alterations in lipid metabolism may account for the increased enzymatic activity of renin in uremic plasma. Increased PRR may be related to the deficiency of a normally occurring renin inhibitor.

Angiotensin I↗
PubMed1980

Studies on the pathogenesis of Bartter's syndrome.

There is no agreement concerning the primary pathogenetic event leading to Bartter's syndrome. Free water clearance and distal fractional chloride reabsorption were abnormally low in our patient with Bartter's syndrome. This series of investigations in this patient with Bartter's syndrome and hypomagnesemia was undertaken to determine if the defect in chloride transport in the ascending limb and the associated renal potassium wasting was specifically related to potassium depletion, increased prostaglandin production or magnesium depletion. Neither potassium repletion, indomethacin administration nor magnesium repletion had an effect on the defect in free water clearance or in distal fractional chloride reabsorption. However, magnesium infusion eliminated renal potassium wasting. These observations suggest that the proximate cause of Bartter's syndrome in this patient is a primary defect in the reabsorption of sodium chloride in the ascending limb and not renal potassium wasting. however, hypomagnesemia may contribute to the renal potassium wasting seen in this syndrome.

Adult↗
PubMed1980

Inhibition of renin secretion by HCl is related to chloride in both dog and rat.

To determine if inhibition of renin release by HCl is related to acidosis or to Cl-, the effects of peripheral venous infusions of HCl and H2SO4 on plasma renin activity (PRA) were compared in the dog and the rat. In NaCl-deprived, pentobarbital-anesthetized dogs, either 0.15 M HCl (n = 10) or 0.075 M H2SO4 (n = 7) was infused for 60 min. In 5 of the 10 HCl-infused dogs (group A), urine Cl- excretion increased (P less than 0.01) during HCl infusion. In the remaining five dogs (group B), Cl- excretion did not increase. Cl- excretion also did not increase during H2SO4 infusion. Comparable acidosis was produced in all three groups. PRA decreased (P less than 0.01) in response to HCl in group A but did not change (P greater than 0.8) in group B HCl-infused dogs or in H2SO4-infused dogs. In NaCl-deprived, anesthetized rats, PRA was suppressed (P less than 0.05) by HCl (from 40.6 +/- 9.4 to 27.4 +/- 5.3 ng . ml-1 . h-1 (SE)) but not H2SO4 (from 37.1 +/- 4.2 to 37.0 +/- 6.3 ng . ml-1 . h-1), despite comparable acidosis. Cl- excretion increased only in HCl-infused rats. In conclusion, inhibition of PRA by acute infusion of HCl is specifically related to Cl-.

Animals↗
PubMed1980

Renin, aldosterone and cortisol in the thoroughbred horse.

To assess the renin-aldosterone system in a large mammal, simultaneous morning activities of plasma renin and concentrations of aldosterone and cortisol were measured in 25 thoroughbred horses. Renin was relatively low in all horses (0.16 +/- 0.02 (S.E.M.) ng angiotensin I/ml per h), levels of aldosterone in plasma were 527 +/- 130 pmol/1 and levels of cortisol in plasma were 141 +/- 11 nmol/l. Levels of aldosterone were significantly correlated with levels of renin in all horses (r = 0.62, P less than 0.001) but not with those of cortisol, and renin was negatively correlated with age in male horses (r = -0.54, P less than 0.05). Horse plasma renin had a pH optimum of 6.0. These data suggest that the thoroughbred horse has a functioning renin-aldosterone system characterized by levels of plasma renin activity that are much lower relative to those of other mammalian species.

Aldosterone↗