Long-term cardiovascular role of nitric oxide in conscious rats.

The goal of this study was to determine the arterial pressure and renal excretory responses to a continuous intravenous infusion of 7.4 nmol/kg per minute of the nitric oxide synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in conscious rats. Studies were conducted in six groups of Sprague-Dawley rats with indwelling arterial and venous catheters over periods lasting 12 to 26 days.

Exaggerated pressor and chronotropic response to chronic hyperinsulinemia in SH versus WKY rats.

Insulin resistance and the sympathetic nervous system have been suggested to be important factors in the blood pressure response to hyperinsulinemia. This study was designed to investigate whether the response to chronic hyperinsulinemia in 14-week-old SH rats (n = 6), which are reported to be insulin resistant and to have a hyperresponsive sympathetic nervous system, would differ from that in WKY rats (n = 5). Mean arterial pressure (MAP) and heart rate (HR) were monitored 19 h/day by computer.

High-fructose diet does not raise 24-hour mean arterial pressure in rats.

High intakes of the simple sugars--glucose, sucrose, and fructose--have been reported to raise significantly systolic pressure in rats. It is not clear, however, if under those conditions the acute measurement of blood pressure, especially with the tail-cuff technique, represents accurately the effect of the diet on mean arterial pressure throughout the day. In this study, 15 Sprague-Dawley rats (approximately 325 g) were chronically instrumented with arterial and venous catheters and placed on a diet containing 61% vegetable starch and 5% dextrose; seven rats remained on this diet throughout the study.

Obesity-induced hypertension. Renal function and systemic hemodynamics.

This study examined the control of renal hemodynamics and tubular function, as well as systemic hemodynamics, during obesity-induced hypertension in chronically instrumented conscious dogs. Mean arterial pressure, cardiac output, and heart rate were monitored 24 hours a day using computerized methods, water and electrolyte balances were measured daily, and renal hemodynamics were measured each week during the control period and 5 weeks of a high-fat diet. After 7 to 10 days of control measurements, 0.

Chronic angiotensin-converting-enzyme inhibition improves cardiac output and fluid balance during heart failure.

The purpose of this study was to examine the sequential changes in renal and cardiovascular function produced by chronic Benazepril administration at different stages of heart failure in dogs. Heart failure was produced by rapid ventricular pacing in five dogs with a normally functioning renin-angiotensin system (angiotensin normal, AN) and six dogs chronically administered the angiotensin-converting-enzyme inhibitor (ACEI) Benazepril. After 7 days of pacing, cardiac output was significantly higher and total peripheral resistance (TPR) lower in the ACEI compared with the AN dogs.

Insulin resistance, hyperinsulinemia, and obesity-associated hypertension.

Recent work to elucidate the cause of obesity-associated hypertension has focused on insulin resistance and hyperinsulinemia. A significant amount of epidemiologic and correlational evidence suggests a link between these factors and obesity-associated hypertension, and acute insulin infusion studies have revealed renal, neural, and cardiovascular effects of this hormone that, if maintained chronically, could cause hypertension. However, correlations and acute effects may not reliably predict a chronic cause-and-effect relationship, and the fundamental question of whether chronic increases in plasma insulin concentration per se can produce a sustained increase in arterial pressure has not been completely resolved.

Comparison of renal actions of urodilatin and atrial natriuretic peptide.

A 32-amino acid atrial natriuretic peptide (ANP)-like peptide, putatively synthesized by the kidney, has recently been isolated from human urine. This peptide, urodilatin (Uro), is structurally similar to the 28-amino acid ANP, suggesting that they might have similar actions on renal fluid and electrolyte excretion. The purpose of this study was to characterize the direct renal actions of low doses of Uro infusion and to compare them with the effects of equimolar intrarenal infusions of either ANP or the 24-amino acid atriopeptin III (AP III).

Pressure natriuresis and angiotensin II in reduced kidney mass, salt-induced hypertension.

In normal subjects, high sodium intake causes little change in mean arterial pressure (MAP). However, MAP is sodium sensitive after reduction of kidney mass. The present study examined the role of increased renal artery pressure and decreased angiotensin II (ANG II) formation in maintaining sodium balance during high sodium intake in dogs with reduced kidney mass.

Hypertension during chronic hyperinsulinemia in rats is not salt-sensitive.

The goal of this study was to examine the chronic blood pressure and renal actions of insulin in conscious rats and to determine whether the blood pressure response to insulin is salt-sensitive. The effects of chronic hyperinsulinemia were examined in three groups of Sprague-Dawley rats given low sodium (LS rats, 0.6 meq/day), normal sodium (NS rats, 3.

Obesity-associated hypertension. Hyperinsulinemia and renal mechanisms.

Hyperinsulinemia and insulin resistance have been postulated to link obesity and hypertension. Evidence supporting this concept derives mainly from epidemiological studies showing a correlation between insulin resistance, hyperinsulinemia, and blood pressure and from short-term studies suggesting that insulin has renal and cardiovascular actions that, if sustained, could elevate blood pressure. However, a cause-and-effect relation between insulin and hypertension has not been clearly established.

Chronic intrarenal hyperinsulinemia does not cause hypertension.

Hyperinsulinemia has been postulated to link obesity and hypertension via the antinatriuretic actions of insulin. The main goal of this study was to quantitate the importance of the direct intrarenal actions of insulin, independent of systemic effects, in altering blood pressure and renal function. This was accomplished by determining the responses to chronic intrarenal insulin infusion in uninephrectomized, chronically instrumented conscious dogs maintained on a 74 meq/day sodium intake.

Sustained hyperinsulinemia increases arterial pressure in conscious rats.

A large body of correlational evidence relating plasma insulin levels and arterial pressure in obese hypertensives suggests that hyperinsulinemia may play a causal role in the development of hypertension in these subjects. However, experimental evidence supporting the ability of increased plasma insulin per se to increase blood pressure is lacking. The goal of this study was to determine the effect of hyperinsulinemia on mean arterial pressure and renal electrolyte excretion in eight conscious rats.

The hemodynamic response to chronic hyperinsulinemia in conscious dogs.

This study describes the hemodynamic effects of chronic hyperinsulinemia in seven normal dogs. Insulin infused at 1 mU/kg/min together with glucose at 14 mg/kg/min for 7 days increased fasting plasma insulin concentration approximately six-fold. Plasma glucose concentration was unchanged on day 1 but was below control on day 6.

Atrial natriuretic factor and blood pressure control: role of sodium and aldosterone.

This study examined the long-term actions of atrial natriuretic factor (ANF), at physiological levels, on renal function and mean arterial pressure (MAP) and the importance of Na intake and the renin-angiotensin-aldosterone system in modulating those effects. After a control period, ANF was infused intravenously at a rate of 10 ng.kg-1.

Intrarenal atrial natriuretic peptide infusion lowers arterial pressure chronically.

Chronic intravenous infusions of atrial natriuretic peptide (ANP) have been shown to lower mean arterial pressure (MAP) in both normal and hypertensive animals. However, the importance of the renal actions of ANP in mediating this hypotension is unknown. This study was designed to determine whether physiological or pathophysiological increases in intrarenal ANP levels influence long-term control of arterial pressure.

Atrial natriuretic peptide induces sustained natriuresis in conscious dogs.

Although acute infusions of atrial natriuretic peptide (ANP) often cause natriuresis, these effects are not sustained, possibly because of reductions in arterial pressure or other compensatory adaptations. The aim of this study was to determine whether physiological increases in intrarenal ANP levels cause sustained natriuresis if changes in arterial pressure and other neurohumoral influences that might obscure the renal responses are controlled. Changes in renal function were quantitated during chronic unilateral renal arterial infusion of ANP at rates of 1, 2, and 4 ng.

Abnormal pressure natriuresis. A cause or a consequence of hypertension?

In all forms of chronic hypertension, the renal-pressure natriuresis mechanism is abnormal because sodium excretion is the same as in normotension despite the increased blood pressure. However, the importance of this resetting of pressure natriuresis as a cause of hypertension is controversial. Theoretically, a resetting of pressure natriuresis could necessitate increased blood pressure to maintain sodium balance or it could occur secondarily to hypertension.

Chronic hyperinsulinemia and blood pressure. Interaction with catecholamines?

Although hyperinsulinemia and increased adrenergic activity have been postulated to be important factors in obesity-associated hypertension, a cause and effect relation between insulin, catecholamines, and hypertension has not been established. The aim of this study was to determine whether chronic hyperinsulinemia, comparable with that found in obese hypertensive patients, causes hypertension in normal dogs, increases plasma catecholamines, or potentiates the blood pressure effects of norepinephrine. In six normal dogs, insulin infusion (1.

ANF and postprandial control of sodium excretion in dogs with compensated heart failure.

The changes in plasma immunoreactive atrial natriuretic factor (iANF) and urinary Na excretion that occur in response to an oral load of Na and to infusion of synthetic atrial natriuretic factor (ANF) were examined in conscious dogs with an arteriovenous (AV) fistula and chronic compensated high-output heart failure. After ingestion of a meal containing 125 meq Na, plasma iANF and right atrial pressure increased from high basal levels of 506 +/- 46 pg/ml and 96 +/- 5 mmH2O to peak responses of 728 +/- 43 pg/ml (P less than 0.05) and 104 +/- 6 mmH2O (P less than 0.

Aldosterone and renin inhibition by atrial natriuretic factor in potassium-loaded rats.

This study was designed to determine the effects of synthetic rat atrial natriuretic factor (ANF) on plasma renin activity (PRA) and aldosterone secretion in separate groups of normal and potassium-loaded anesthetized rats. Control rats were fed a normal diet of sodium and potassium and had base-line levels of PRA and aldosterone secretion of 25 +/- 3 ng angiotensin I (ANG I).ml-1.

DOCA administration and atrial natriuretic factor in dogs with chronic heart failure.

The chronic reserve for the secretion of atrial natriuretic factor (ANF) was studied in conscious dogs with an arteriovenous (a-v) fistula, a model of high-output heart failure. After the first 7 days of marked sodium retention after creation of the a-v fistula, the animals regained sodium balance for the subsequent 3 wk. This compensatory natriuresis occurred in the presence of significant increases in right atrial pressure and was associated with marked and sustained elevations in plasma ANF and with the return of plasma renin and aldosterone to base-line values.

Cardiovascular and renal effects of calcitonin gene-related peptide in hypertensive dogs.

The systemic cardiovascular and renal effects of synthetic beta-human calcitonin gene-related peptide (beta-hCGRP) were examined in conscious normotensive and one-kidney one-clip (1K-1C) hypertensive dogs. beta-hCGRP was infused intravenously at 10 and 50 ng/kg/min for 75-min periods each. Mean arterial pressure did not change significantly (p greater than 0.

Renal hemodynamic response to intrarenal infusion of calcitonin gene-related peptide in dogs.

The renal hemodynamic and excretory effects of intrarenal infusions of synthetic beta-human calcitonin gene-related peptide (beta-hCGRP) were examined in normal sodium replete dogs (Group 1, n = 6), in sodium replete dogs pretreated with indomethacin (Group 2, n = 6), and in sodium deplete dogs (Group 3, n = 5). In all groups of anesthetized dogs beta-hCGRP was infused at 5 and 10 ng.kg-1.

Effects of calcitonin gene-related peptide on renal blood flow in the rat.

The effects of alpha-rat calcitonin gene-related peptide (alpha-rCGRP) on systemic and renal hemodynamics and on renal electrolyte excretion were examined in normal anesthetized rats. In one group of rats (n = 7), infusions of alpha-rCGRP at doses of 10, 50, 100, and 500 ng/kg/min for 15 min each produced dose-related and significant decreases in mean arterial pressure from a control of 130 +/- 3 mm Hg to a maximal depressor response of 91 +/- 2 mm Hg. During the first three doses of alpha-rCGRP, renal blood flow progressively and significantly increased from a control of 5.

Aldosterone and renin inhibition by physiological levels of atrial natriuretic factor.

This study was designed to examine, in the rat, the inhibition of renin release and aldosterone secretion by physiological plasma levels of atrial natriuretic factor (ANF). Intravascular volume expansion over 30 min with donor blood equal to 3% body weight increased plasma ANF concentration from a base line of 216 +/- 28 to 1,590 +/- 240 pg/ml (P less than 0.001) in sodium-replete rats.