The Release of Renal Prostaglandins during Saline Infusion in Normal and Hypertensive Subjects

1975 ◽  
Vol 49 (5) ◽  
pp. 459-463 ◽  
Author(s):  
N. Papanicolaou ◽  
M. Safar ◽  
A. Hornych ◽  
F. Fontaliran ◽  
Y. Weiss ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Flow ◽  
Chloride Solution ◽  
Renal Plasma Flow ◽  
Saline Infusion ◽  
Urinary Output ◽  
Prostaglandin Release ◽  
Before And After ◽  
Solution Saline ◽  
Pressure Changes

1. Renal venous prostaglandin concentrations (PGA, PGE and PGF) were determined, together with renal plasma flow, urinary output and blood pressure changes, before and after infusion of sodium chloride solution (saline) in four normotensive and three hypertensive subjects. 2. No changes in blood pressure and in glomerular filtration rate were observed. 3. Saline infusion induced a significant increase in renal venous PGA and PGE, and also in total and non-cortical renal plasma flow and urinary output. There was an insignificant increase in renal venous PGF. 4. These findings show that prostaglandin release after saline infusion is associated with changes in renal blood flow and suggest that the natriuretic and diuretic effect of saline could be the result of prostaglandin release.

RENAL FUNCTION AND KIDNEY SIZE FOLLOWING HYPOPHYSECTOMY IN MAN

1965 ◽  
Vol 48 (3) ◽  
pp. 348-354 ◽  
Author(s):  
Thomas Falkheden ◽  
Ingmar Wickbom
Keyword(s):  
Renal Function ◽  
Diabetic Retinopathy ◽  
Glomerular Filtration Rate ◽  
Plasma Flow ◽  
Mammary Carcinoma ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Kidney Weight ◽  
Kidney Size ◽  
Before And After

ABSTRACT Measurements of glomerular filtration rate (GFR) and renal plasma flow (RPF) were performed in close connection with roentgenographic estimation of kidney size, before and after hypophysectomy, in 10 patients (four cases of metastatic mammary carcinoma, five cases of diabetic retinopathy and one case of acromegaly). Hypophysectomy was regularly followed by a decrease in GFR and RPF. In most cases, a reduction in the roentgenographic kidney size was also observed. However, the changes in the roentgenographic kidney size and calculated kidney weight after hypophysectomy were smaller and occurred at a slower rate than the alterations in GFR and RPF. The results favour the view that, primarily, the decrease in GFR and RPF following hypophysectomy is essentially functional rather than due to a reduced kidney mass.

scholarly journals DOES GENDER INFLUENCE RISK FOR ORTHOSTATIC HYPOTENSION IN OLDER ADULTS WITH SARCOPENIA?

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S682-S682
Author(s):  
Melissa J Benton ◽  
Amy L Silva-Smith ◽  
Jefferson M Spicher
Keyword(s):  
Blood Pressure ◽  
Older Adults ◽  
Systolic Blood Pressure ◽  
Orthostatic Hypotension ◽  
Lean Mass ◽  
Bioelectrical Impedance ◽  
Early Morning ◽  
Postural Changes ◽  
Before And After ◽  
Pressure Changes

Abstract Older adults with sarcopenia may be at risk for unstable postural blood pressure due to diminished lean mass that plays a role in maintaining fluid volume. Males have greater lean mass, so risk may be mediated by gender. We compared postural blood pressure changes in older men (77.1 ± 2.0 years; n = 15) and women (79.6 ± 2.0 years; n = 13) with sarcopenia before and after an overnight fast. Sarcopenia was defined using the Lean Mass Index (males ≤ 19.0 kg/m2; females ≤ 15.0 kg/m2). Body composition was measured using multi-frequency bioelectrical impedance, and blood pressure was measured lying, sitting, and standing. On Day 1 (normally hydrated) there were significant drops in systolic blood pressure, with an overall decrease of -9.1 ± 2.2 mmHg (p < 0.001) between lying and standing. On Day 2 (overnight fast), postural changes were more profound, with an overall decrease of -14.1 ± 2.8 mmHg (p < 0.001). However, when compared by gender, postural changes between lying and standing remained significant but did not differ between men and women (Day 1: men -8.9 ± 2.5 vs. women -9.3 ± 2.5 mmHg; Day 2: men -14.6 ± 4.6 vs. women -13.6 ± 3.1 mmHg). On both days diastolic blood pressure remained stable. In this group of older adults, significant decreases in postural systolic blood pressure were observed in the early morning fasted condition, increasing the risk for orthostatic hypotension (drop in systolic blood pressure -20.0 mmHg). Interestingly, gender did not influence risk.

Mechanism of Early and Chronic Experimental Renal Hypertension as Tested by CCK-179

1956 ◽  
Vol 186 (1) ◽  
pp. 161-166 ◽  
Author(s):  
Irene H. Oyen
Keyword(s):  
Blood Pressure ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Repeated Administration ◽  
Maximal Effect ◽  
Renal Effects ◽  
Experimental Renal Hypertension

The effects on blood pressure and renal clearances of a combination of dihydrogenated ergot alkaloids, CCK-179, were studied in normal dogs and dogs with experimental renal (Goldblatt) hypertension. The drug was observed to have a maximal effect at 0.012 mg/kg, about one twelfth to one sixteenth the dose recommended in the literature. In normal dogs the drug causes a slight fall in blood pressure, a moderate decrease in glomerular filtration rate (creatinine clearance) and a pronounced decrease in renal plasma flow (PAH clearance), hemodynamic effects resembling those seen in man. After repeated administration of the drug, the renal effects are of greater magnitude in these dogs. In hypertensive dogs, CCK-179 causes blood pressure to approach normal levels. In the early weeks of hypertension, the renal effects of the drug are similar to those seen in normals but as hypertension increases in duration up to 55 weeks, the decreases in filtration rate and plasma flow become progressively smaller. This could indicate that in chronic experimental renal hypertension the high peripheral resistance is maintained at least in part by increased activity of the sympathetic nervous system rather than by the action of the components of the renal humoral pressor system.

Familial Hypertension and Hormonal Profile, Renal Haemodynamics and Body Fluids of Young Normotensive Subjects

1978 ◽  
Vol 55 (s4) ◽  
pp. 367s-371s ◽  
Author(s):  
G. Bianchi ◽  
G. B. Picotti ◽  
G. Bracchi ◽  
D. Cusi ◽  
M. Gatti ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Renal Plasma Flow ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Significant Negative Correlation ◽  
Renin Activity ◽  
Compensatory Mechanism ◽  
Normotensive Subjects

1. Almost all the factors that may cause a rise in blood pressure are, in turn, influenced by the increase in blood pressure per se. Thus any primary involvement of one or more of these factors in the pathogenesis of essential hypertension must be evaluated before or during the development of hypertension. 2. Young normotensive subjects both of whose parents are hypertensive have a much higher probability of developing hypertension than those whose parents are both normotensive. 3. The following measurements were made in 56 subjects of the first group (both parents hypertensive) and 35 of the second group (both parents normotensive), matched for age, sex and body surface area: renal plasma flow and glomerular filtration rate, using p-aminohippurate and inulin clearance; 24 h urinary excretion of aldosterone, protein and electrolytes; plasma renin activity; plasma volume. Plasma catecholamines and cardiac index were also measured in 26 subjects of the first group and 25 subjects of the second group using a radioenzymic method and echocardiography. 4. All these factors were similar in the two groups except that renal plasma flow was higher in the first group (767·2 ± 30 versus 650·7 ± 17 ml/min, P < 0·01). Plasma renin activity tended to be lower in subjects with a higher renal plasma flow, but there was no significant negative correlation between the two factors. 5. The possibility that the higher renal plasma flow in subjects with a high probability of developing hypertension is a compensatory mechanism for a primary intrarenal defect is discussed.

Ouabain prevents loss of autoregulation in rat pial arterioles caused by reoxygenation after a brief hypoxic episode

1989 ◽  
Vol 67 (5) ◽  
pp. 423-427 ◽  
Author(s):  
J. Kettler ◽  
B. Y. Ong ◽  
D. Bose
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Protective Effects ◽  
Cranial Window ◽  
Arterial Blood ◽  
Hypoxic Episode ◽  
Electrogenic Sodium Pump ◽  
Before And After ◽  
Pressure Changes ◽  
Arteriolar Diameter

Pial arteriolar diameter changes inversely with changes in systemic arterial blood pressure. Such changes are consistent with autoregulatory functions. These responses are reduced by a brief period of hypoxia followed by reoxygenation. By using an open cranial window preparation we assessed the changes in pial arteriolar diameters during blood pressure changes in rats induced by hemorrhage and reinfusion of blood, before and after a brief period of hypoxia. The slopes of the changes in pial arteriolar diameter as a function of mean arterial blood pressure were −0.47 ± 0.26 μm/mmHg (mean ± SD; 1 mmHg = 133.3 Pa) before hypoxia and −0.11 ± 0.23 μm/mmHg after hypoxia in the untreated rats. In ouabain-treated rats, corresponding slopes were −0.42 ± 0.24 and −0.46 ± 0.22 μm/mmHg. The observed protective effects of ouabain might be a blockade of the Na–K pump in the sarcolemma of the vascular smooth muscle.Key words: vascular smooth muscle, electrogenic sodium pump, metabolic inhibition.

scholarly journals Knockdown of parathyroid hormone related protein in smooth muscle cells alters renal hemodynamics but not blood pressure

2013 ◽  
Vol 305 (3) ◽  
pp. F333-F342 ◽  
Author(s):  
Denis Raison ◽  
Catherine Coquard ◽  
Mazène Hochane ◽  
Jacques Steger ◽  
Thierry Massfelder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Parathyroid Hormone ◽  
Plasma Flow ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Related Protein ◽  
Filtration Fraction ◽  
Parathyroid Hormone Related Protein

Parathyroid hormone-related protein (PTHrP) belongs to vasoactive factors that regulate blood pressure and renal hemodynamics both by reducing vascular tone and raising renin release. PTHrP is expressed in systemic and renal vasculature. Here, we wanted to assess the contribution of vascular smooth muscle cell endogenous PTHrP to the regulation of cardiovascular and renal functions. We generated a mouse strain ( SMA-CreER T2/ PTHrP L2/L2 or premutant PTHrP SM−/−), which allows temporally controlled, smooth muscle-targeted PTHrP knockdown in adult mice. Tamoxifen treatment induced efficient recombination of PTHrP-floxed alleles and decreased PTHrP expression in vascular and visceral smooth muscle cells of PTHrP SM−/− mice. Blood pressure remained unchanged in PTHrP SM−/− mice, but plasma renin concentration and creatinine clearance were reduced. Renal hemodynamics were further analyzed during clearance measurements in anesthetized mice. Conditional knockdown of PTHrP decreased renal plasma flow and glomerular filtration rate with concomitant reduction in filtration fraction. Similar measurements were repeated during acute saline volume expansion. Saline volume expansion induced a rise in renal plasma flow and reduced filtration fraction; both were blunted in PTHrP SM−/− mice leading to impaired diuresis. These findings show that endogenous vascular smooth muscle PTHrP controls renal hemodynamics under basal conditions, and it is an essential factor in renal vasodilation elicited by saline volume expansion.

Differential effect of T-type voltage-gated Ca2+ channel disruption on renal plasma flow and glomerular filtration rate in vivo

2014 ◽  
Vol 307 (4) ◽  
pp. F445-F452 ◽  
Author(s):  
Anne D. Thuesen ◽  
Henrik Andersen ◽  
Majken Cardel ◽  
Anja Toft ◽  
Steen Walter ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Voltage Gated

Voltage-gated Ca2+ (Cav) channels play an essential role in the regulation of renal blood flow and glomerular filtration rate (GFR). Because T-type Cav channels are differentially expressed in pre- and postglomerular vessels, it was hypothesized that they impact renal blood flow and GFR differentially. The question was addressed with the use of two T-type Cav knockout (Cav3.1−/− and Cav3.2−/−) mouse strains. Continuous recordings of blood pressure and heart rate, para-aminohippurate clearance (renal plasma flow), and inulin clearance (GFR) were performed in conscious, chronically catheterized, wild-type (WT) and Cav3.1−/− and Cav3.2−/− mice. The contractility of afferent and efferent arterioles was determined in isolated perfused blood vessels. Efferent arterioles from Cav3.2−/− mice constricted significantly more in response to a depolarization compared with WT mice. GFR was increased in Cav3.2−/− mice with no significant changes in renal plasma flow, heart rate, and blood pressure. Cav3.1−/− mice had a higher renal plasma flow compared with WT mice, whereas GFR was indistinguishable from WT mice. No difference in the concentration response to K+ was observed in isolated afferent and efferent arterioles from Cav3.1−/− mice compared with WT mice. Heart rate was significantly lower in Cav3.1−/− mice compared with WT mice with no difference in blood pressure. T-type antagonists significantly inhibited the constriction of human intrarenal arteries in response to a small depolarization. In conclusion, Cav3.2 channels support dilatation of efferent arterioles and affect GFR, whereas Cav3.1 channels in vivo contribute to renal vascular resistance. It is suggested that endothelial and nerve localization of Cav3.2 and Cav3.1, respectively, may account for the observed effects.

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