Renal Responses to Acute Elevation of Blood Pressure in Dogs

2015 ◽  
pp. 198-202
Author(s):  
Fredrik Kiil
Keyword(s):  
Blood Pressure ◽  
Acute Elevation ◽  
Renal Responses

Effect of Ketoprofen on Blood Pressure, Endocrine and Renal Responses to Chronic Dosing with Captopril in Patients with Essential Hypertension

1992 ◽  
Vol 1 (3) ◽  
pp. 162-167 ◽  
Author(s):  
Jean R. Cusson ◽  
Patrick Du Souich ◽  
Patrick Le Morvan ◽  
Gaétan Thibault ◽  
Robert Phillips ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Renal Responses

Reduced renal responses to an acute saline load in obese Zucker rats

1991 ◽  
Vol 261 (3) ◽  
pp. R712-R718 ◽  
Author(s):  
D. W. Zeigler ◽  
K. P. Patel
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Urine Flow ◽  
Reflex Response ◽  
Zucker Rats ◽  
Zucker Rat ◽  
Obese Zucker Rat ◽  
Obese Zucker Rats ◽  
Renal Responses

The purpose of this study was to determine if the reflex response to a saline load is altered in the obese Zucker rat. The obese Zucker rat is a genetic model of obesity and insulin-resistant diabetes that has been reported to have high blood pressure. We examined the reflux renal responses to volume expansion in both anesthetized obese and lean Zucker rats. Initial blood pressure was significantly elevated in the obese Zucker rats compared with the lean controls. Urine flow and sodium excretion from innervated and denervated kidneys were measured before and after volume expansion with normal saline. Volume expansion resulted in significantly less urine flow and sodium excretion in the obese than the lean Zucker rats. This response was evident in both the intact and denervated kidneys. Rats were then infused with atrial natriuretic peptide (ANP) to determine if natriuretic and diuretic responses were altered in these rats. The diuretic action of ANP was not significantly reduced in the obese Zucker rat. However, the natriuretic action of ANP was significantly attenuated in the obese rats. These results indicate that the reflux response to an acute saline load is attenuated in the obese Zucker rat and that this decreased response may be due to a reduction in the direct action of ANP on the kidney.

PRESSOR RESPONSIVENESS FOLLOWING ACUTE ELEVATION OF SODIUM IN THE RAT

1957 ◽  
Vol 35 (1) ◽  
pp. 327-331 ◽  
Author(s):  
Sydney M. Friedman ◽  
W. A. Webber ◽  
J. D. Jamieson ◽  
Constance L. Friedman
Keyword(s):  
Blood Pressure ◽  
Sodium Acetate ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
High Plasma ◽  
Potassium Citrate ◽  
Plasma Sodium ◽  
Adult Rats ◽  
Sodium Potassium ◽  
Acute Elevation

In order to test the effects of various ions on pressor responsiveness, groups of adult rats were infused with solutions containing sufficient sodium, potassium, calcium, or magnesium to elevate the plasma concentration of these ions. The infusions were completed within 5 minutes and in no case was more than 0.5 ml. injected. The test solutions used were sodium acetate, potassium citrate, calcium chloride, and magnesium sulphate. Control solutions of ammonium acetate, ammonium sulphate, sodium chloride, and sucrose were also infused. In no case was the amount of salt infused sufficient to affect the blood pressure during the infusion. The blood pressure response to 1 γ of norepinephrine or to 20 mU. of pitressin was recorded before infusion and again at the end of the infusion. A significant effect was observed only with sodium acetate. This consisted of a profound suppression of the ordinary pressor response to both norepinephrine and pitressin. The effect was not due to the acetate ion and hence may be specifically referable to the high plasma sodium. These results support our previous conclusions that pressor responsiveness and sodium mobility are causally connected.

Hormonal and renal responses to converting enzyme inhibition during maximal exercise

1987 ◽  
Vol 63 (5) ◽  
pp. 1796-1800 ◽  
Author(s):  
C. E. Wade ◽  
S. R. Ramee ◽  
M. M. Hunt ◽  
C. J. White
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Maximal Exercise ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Renal Handling ◽  
Renal Responses ◽  
Captopril Treatment

The role of angiotensin II in the hormonal and renal responses to maximal exercise was investigated by using the angiotensin-converting enzyme inhibitor captopril. Nine male subjects performed a standardized maximal treadmill test with and without acute captopril treatment (25 mg orally). At rest, captopril elevated plasma renin activity and lowered aldosterone levels. With maximal exercise, captopril treatment reduced the increase in mean arterial blood pressure by 8 mmHg and the increase in plasma renin activity by 3.0 ng ANG I.ml-1.h-1. The responses of adrenocorticotropin (ACTH), cortisol, and vasopressin to maximal exercise were not altered by captopril treatment. Although aldosterone levels were reduced at rest with captopril, during maximal exercise no difference was noted between treatments. Captopril treatment had no effects on the renal handling of salts or water during exercise. In conclusion, angiotensin II plays a role in the increase in mean blood pressure during maximal exercise in normal subjects but has no effect on the exercise responses of ACTH, vasopressin, and aldosterone or on the renal handling of salts and water.

Acute elevation of triglycerides increases left ventricular contractility and alters ventricular-vascular interaction

2011 ◽  
Vol 301 (1) ◽  
pp. H123-H128 ◽  
Author(s):  
David J. Holland ◽  
Dominique Erne ◽  
Karam Kostner ◽  
Rodel Leano ◽  
Brian A. Haluska ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Strain Rate ◽  
Free Fatty Acids ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Fat Emulsion ◽  
Intravenous Fat Emulsion ◽  
Acute Elevation

Acute elevation of circulating lipids, such as the postprandial state, contributes to increased cardiovascular risk. However, the effect of acutely elevated triglycerides on arterial and left ventricular function is not completely understood. We aimed to assess whether an acute increase in triglycerides affects ventricular-vascular interaction. Fifteen healthy men (age, 49 ± 8 yr) underwent blinded, randomized infusion of saline and intravenous fat emulsion to acutely raise plasma triglycerides. All subjects underwent both randomization trials, in random order on two separate days. Ventricular-vascular interaction measures were recorded by tonometry (central blood pressure) and echocardiography (left ventricular volumes, strain, and strain rate) at baseline and after 1 h infusion. Net ventricular-vascular interaction was defined by the effective arterial elastance ( EA)-to-left ventricular end-systolic elastance ( ELV) ratio ( EA/ ELV). When compared with saline, the infusion of intravenous fat emulsion increased triglycerides and free fatty acids (Δ P < 0.001 for both) and improved left ventricular contractility (Δ ELV, end-systolic volume and strain rate; P < 0.05 for all). However, arterial function was unchanged (Δ EA, brachial and central blood pressure; P > 0.05 for all). Overall, EA/ ELV was decreased by an infusion of intravenous fat emulsion ( P = 0.004) but not saline ( P > 0.05, P = 0.001 for Δ between trials). We conclude that intravenous fat emulsion and acute elevation of blood lipids (including triglycerides and free fatty acids) alter ventricular-vascular interaction by increasing left ventricular contractility without affecting arterial load. These findings may have implications for cardiovascular responses to parenteral nutrition.

scholarly journals Effect of Sodium Balance on Arterial Blood Pressure and Renal Responses to Prostaglandin A1in Man

1973 ◽  
Vol 33 (5) ◽  
pp. 539-546 ◽  
Author(s):  
LAWRENCE R. KRAKOFF ◽  
DAISY DE GUIA ◽  
NICHOLAS VLACHAKIS ◽  
JENNIE STRICKER ◽  
MARVIN GOLDSTEIN
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sodium Balance ◽  
Arterial Blood ◽  
Renal Responses

Aldosterone sensitivity: an opportunity for investigation into the pathogenesis of hypertension

2021 ◽  
Author(s):  
Zachary Gray ◽  
Wanzhu Tu ◽  
Glenn M Chertow ◽  
Vivek Bhalla
Keyword(s):  
Blood Pressure ◽  
Clinical Studies ◽  
Randomized Trials ◽  
Science Studies ◽  
Differential Sensitivity ◽  
Outcome Variable ◽  
Black Race ◽  
Tissue Responses ◽  
Urine Potassium ◽  
Renal Responses

Aldosterone sensitivity is defined as an outcome variable for a given circulating level of aldosterone. In basic and translational studies, this has been measured in differential tissue responses, e.g. lower urine sodium and higher urine potassium, as an index of renal response; and in clinical studies has been measured in differential blood pressure. This concept of aldosterone sensitivity disrupts the conventional wisdom of the renin-angiotensin-aldosterone system and has the potential to uncover novel mechanisms of hypertension. We review basic and translational science studies that uncovered differential renal responses to aldosterone and connect this earlier work to more recent observational and randomized trials that have demonstrated differential blood pressure for a given level of aldosterone in healthy and hypertensive subjects. Black race and age are associated with higher aldosterone sensitivity and blood pressure. We also discuss gaps in the field and how future basic and clinical studies can inform mechanisms of differential sensitivity.

Sign in / Sign up

Export Citation Format

Share Document