Dietary calcium decreases blood pressure without decreasing renal vascular resistance or altering the response to NO blockade

1997 ◽  
Vol 130 (6) ◽  
pp. 627-634 ◽  
Author(s):  
John C. Passmore ◽  
Daniel C. Hatton ◽  
David A. Mccarron
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Dietary Calcium ◽  
Renal Vascular Resistance ◽  
Renal Vascular

Limb tourniquet and intramuscular clostridial toxin effects on renal function

1962 ◽  
Vol 17 (1) ◽  
pp. 83-86 ◽  
Author(s):  
James F. Nickel ◽  
John A. Gagnon ◽  
Leonard Levine
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Sodium Excretion ◽  
Renal Vascular Resistance ◽  
Arterial Blood ◽  
Hind Limbs ◽  
Renal Changes ◽  
Anesthetized Dogs ◽  
Peripheral Trauma ◽  
Renal Vascular

Eight anesthetized dogs, given Clostridium perfringens type A toxic filtrate into the hind-limb muscles, showed severe spreading edema, hemoconcentration, marked reduction in para-aminohippurate (PAH) and creatinine clearances, and a rise in the renal vascular resistance. In the first 4 hr sodium excretion fell sharply, and mean arterial blood pressure, slightly. In eight similar dogs venous-occlusive pneumatic tourniquets were applied high on both hind limbs for 90 min. Edema was localized and minimal. Hematocrit was unchanged. PAH and creatinine clearances were extremely low in the second 30-min period of the occlusion but had risen somewhat in the last 30-min period. Sodium excretion was greatly reduced. Arterial pressure and vascular resistance rose very significantly. Upon removal of the tourniquets, PAH and creatinine clearances, blood pressure, and renal vascular resistance returned toward normal. Sodium excretion continued to fall. In many respects the renal changes resulting from two different forms of peripheral trauma are similar. Submitted on August 14, 1959

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

Abnormal Renal Haemodynamics and Renin Suppression in Hypertensive Patients

1970 ◽  
Vol 38 (1) ◽  
pp. 101-110 ◽  
Author(s):  
M. A. D. H. Schalekamp ◽  
M. P. A. Schalekamp-Kuyken ◽  
W. H. Birkenhäger
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Hypertensive Disease ◽  
Filtration Fraction ◽  
Plasma Renin Concentration ◽  
Renal Vascular ◽  
Intravascular Pressure

1. Intra-arterial pressure, renal plasma flow and glomerular filtration rate were estimated in thirty-two patients with benign essential hypertension. In twenty cases plasma renin concentrations were also determined. Variability of blood pressure was estimated by automatic indirect pressure recording. 2. There was an even distribution between high and low values of renal vascular resistance and filtration fraction. Variability of blood pressure was inversely related to renal vascular resistance. 3. In five patients plasma renin concentration was found to be abnormally low both in the recumbent and in the 45° tilt position. 4. Plasma renin concentration was related to renal blood flow, renal vascular resistance, filtration fraction and variability of blood pressure. 5. The results suggest that in hypertension renin release is suppressed by an increase in intravascular pressure at the level of the juxtaglomerularcells. The extent of renin suppression seems to be related to the stage of hypertensive disease.

Inhibition of ROMK blocks macula densa tubuloglomerular feedback yet causes renal vasoconstriction in anesthetized rats

2017 ◽  
Vol 312 (6) ◽  
pp. F1120-F1127 ◽  
Author(s):  
Magali Araujo ◽  
William J. Welch ◽  
Xiaoyan Zhou ◽  
Kathleen Sullivan ◽  
Shawn Walsh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Tubuloglomerular Feedback ◽  
Volume Depletion ◽  
Renal Vasoconstriction ◽  
Compound C ◽  
Altered Blood ◽  
Renal Vascular ◽  
Dose Dependent

The Na+-K+-2Cl− cotransporter (NKCC2) on the loop of Henle is the site of action of furosemide. Because outer medullary potassium channel (ROMK) inhibitors prevent reabsorption by NKCC2, we tested the hypothesis that ROMK inhibition with a novel selective ROMK inhibitor (compound C) blocks tubuloglomerular feedback (TGF) and reduces vascular resistance. Loop perfusion of either ROMK inhibitor or furosemide caused dose-dependent blunting of TGF, but the response to furosemide was 10-fold more sensitive (IC50 = 10−6 M for furosemide and IC50 = 10−5 M for compound C). During systemic infusion, both diuretics inhibited TGF, but ROMK inhibitor was 10-fold more sensitive (compound C: 63% inhibition; furosemide: 32% inhibition). Despite blockade of TGF, 1 h of constant systemic infusion of both diuretics reduced the glomerular filtration rate (GFR) and renal blood flow (RBF) by 40–60% and increased renal vascular resistance (RVR) by 100–200%. Neither diuretic altered blood pressure or hematocrit. Proximal tubule hydrostatic pressures (PPT) increased transiently with both diuretics (compound C: 56% increase; furosemide: 70% increase) but returned to baseline. ROMK inhibitor caused more natriuresis (3,400 vs. 1,600% increase) and calciuresis (1,200 vs. 800% increase) but less kaliuresis (33 vs. 167% increase) than furosemide. In conclusion, blockade of ROMK or Na+-K+-2Cl− transport inhibits TGF yet increases renal vascular resistance. The renal vasoconstriction was independent of volume depletion, blood pressure, TGF, or PPT.

scholarly journals Angiotensin II blockade causes acute renal failure in eNOS-deficient mice

2001 ◽  
Vol 2 (1_suppl) ◽  
pp. S199-S203 ◽  
Author(s):  
Jürgen Schnermann ◽  
Yuning G Huang ◽  
Josie P Briggs
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Vascular Resistance ◽  
Knockout Mice ◽  
Renal Vascular Resistance ◽  
Wild Type ◽  
Arteriolar Tone ◽  
Renal Vascular ◽  
Deficient Mice

Compared with wild-type mice, adult endothelial nitric oxide synthase (eNOS) knockout mice (eight months of age) have increased blood pressure (BP) (126±9 mmHg vs. 100±4 mmHg), and an increased renal vascular resistance (155±16 vs. 65±4 mmHg.min/ml). Renal vascular resistance responses to i.v. administration of noradrenaline were markedly enhanced in eNOS knockout mice. Glomerular filtration rate (GFR) of anaesthetised eNOS -/- mice was 324±57 µl/min gKW, significantly lower than the GFR of 761±126 µl/min.gKW in wild-type mice. AT1-receptor blockade with i.v. candesartan (1—1.5 mg/kg) reduced arterial blood pressure and renal vascular resistance, and increased renal blood flow (RBF) to about the same extent in wild-type and eNOS -/- mice. Candesartan did not alter GFR in wild-type mice (761±126 vs. 720±95 µl/min.gKW), but caused a marked decrease in GFR in eNOS -/- mice (324.5±75.2 vs. 77±18 µl/min.gKW). A similar reduction in GFR of eNOS deficient mice was also caused by angiotensin-converting enzyme (ACE) inhibition. Afferent arteriolar granularity, a measure of renal renin expression, was found to be reduced in eNOS -/- compared with wild-type mice. In chronically eNOS-deficient mice, angiotensin II (Ang II) is critical for maintaining glomerular filtration pressure and GFR, presumably through its effect on efferent arteriolar tone.

Absence of Adrenergic Mediation of Agonist Response to [Sar1,Ala8]Angiotensin II in Conscious Normotensive and Hypertensive Dogs

1979 ◽  
Vol 57 (1) ◽  
pp. 71-81 ◽  
Author(s):  
B. G. Zimmerman
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Intravenous Infusion ◽  
Direct Action ◽  
Renal Vascular Resistance ◽  
Angiotensin Receptors ◽  
Conscious Dog ◽  
Renal Vascular

1. In the conscious normotensive and two-kidney Goldblatt hypertensive dog a transient agonist response to the intravenous infusion of saralasin (1 μg min−1 kg−1) was manifested by a small increase in blood pressure (6–12 mmHg) and 28–30% increase in renal vascular resistance. 2. These increases in blood pressure and renal vascular resistance were unaffected by administration of either phentolamine or guanethidine. 3. The agonist response in the conscious dog is most likely accounted for by a direct action of saralasin on vascular angiotensin receptors.

Reduced autoregulatory effectiveness in adenosine 1 receptor-deficient mice

2006 ◽  
Vol 290 (4) ◽  
pp. F888-F891 ◽  
Author(s):  
S. Hashimoto ◽  
Y. Huang ◽  
J. Briggs ◽  
J. Schnermann
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Blood Pressure Reduction ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Tubuloglomerular Feedback ◽  
Wild Type ◽  
Before And After ◽  
Renal Vascular ◽  
Deficient Mice

Adjustments of renal vascular resistance in response to changes in blood pressure are mediated by an interplay between the myocyte-inherent myogenic and the kidney-specific tubuloglomerular feedback (TGF) mechanisms. Using mice with deletion of the A1 adenosine receptor (A1AR) gene, we tested the prediction that the absence of TGF, previously established to result from A1AR deficiency, is associated with a reduction in the efficiency of autoregulation. In anesthetized wild-type (A1AR+/+) and A1AR-deficient mice (A1AR−/−), glomerular filtration rate (GFR) and renal blood flow (RBF) were determined before and after reducing renal perfusion pressure through a suprarenal aortic clamp. In response to a blood pressure reduction by 15.9 ± 1.34 mmHg in A1AR−/− ( n = 9) and by 14.2 ± 0.9 mmHg in A1AR+/+ mice ( n = 8; P = 0.31), GFR fell by 187.9 ± 37 μl/min and by 72.3 ± 10 μl/min in A1AR−/− and A1AR+/+ mice, respectively ( P = 0.013). Similarly, with pressure reductions of 14.8 ± 1.1 and 13.3 ± 1.5 mmHg in A1AR−/− ( n = 9) and wild-type mice ( n = 8), respectively ( P = 0.43), RBF fell by 0.17 ± 0.02 ml/min in A1AR−/− mice and by only 0.08 ± 0.02 ml/min in wild-type animals ( P = 0.0039). Autoregulatory indexes for both GFR and RBF were significantly higher in A1AR−/− compared with A1AR+/+ mice, indicating reduced regulatory responsiveness in the knockout animals. We conclude that autoregulation of renal vascular resistance is less complete in A1AR-deficient mice, an effect that is presumably related to absence of TGF regulation in these animals.

A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats

2008 ◽  
Vol 294 (6) ◽  
pp. R1847-R1855 ◽  
Author(s):  
Maarten P. Koeners ◽  
Branko Braam ◽  
Dionne M. van der Giezen ◽  
Roel Goldschmeding ◽  
Jaap A. Joles
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Renal Injury ◽  
Renal Vascular Resistance ◽  
Perinatal Exposure ◽  
Hypertensive Rats ◽  
No Donor ◽  
Renal Vascular

Enhancing perinatal nitric oxide (NO) availability persistently reduces blood pressure in spontaneously hypertensive rats. We hypothesize that this approach can be generalized to other models of genetic hypertension, for instance those associated with renal injury. Perinatal exposure to the NO donor molsidomine was studied in fawn-hooded hypertensive (FHH) rats, a model of mild hypertension, impaired preglomerular resistance, and progressive renal injury. Perinatal molsidomine increased urinary NO metabolite excretion at 8 wk of age, i.e., 4 wk after treatment was stopped ( P < 0.05). Systolic blood pressure was persistently reduced after molsidomine (42-wk females: 118 ± 3 vs. 141 ± 5 and 36-wk males: 139 ± 4 vs. 158 ± 4 mmHg; both P < 0.001). Perinatal treatment decreased glomerular filtration rate ( P < 0.05) and renal blood flow ( P < 0.01) and increased renal vascular resistance ( P < 0.05), without affecting filtration fraction, suggesting persistently increased preglomerular resistance. At 4 wk of age natriuresis was transiently increased by molsidomine ( P < 0.05). Molsidomine decreased glomerulosclerosis ( P < 0.05). Renal blood flow correlated positively with glomerulosclerosis in control ( P < 0.001) but not in perinatally treated FHH rats. NO dependency of renal vascular resistance was increased by perinatal molsidomine. Perinatal enhancement of NO availability can ameliorate development of hypertension and renal injury in FHH rats. Paradoxically, glomerular protection by perinatal exposure to the NO donor molsidomine may be due to persistently increased preglomerular resistance. The mechanisms by which increased perinatal NO availability can persistently reprogram kidney function and ameliorate hypertension deserve further study.

Renal vascular effects of epinephrine infusion in the halothane-anesthetized piglet

1994 ◽  
Vol 72 (4) ◽  
pp. 394-396 ◽  
Author(s):  
Keith J. Harrington ◽  
Robert G. Allen ◽  
Jay W. Dewald
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Mean Arterial Blood Pressure ◽  
Renal Vascular Resistance ◽  
Epinephrine Infusion ◽  
Arterial Blood ◽  
Renal Vascular

The objective of this study was to determine the dose–response effects of epinephrine, given by systemic intravenous infusion to the halothane-anesthetized newborn piglet, on renal blood flow, mean arterial blood pressure, and renal vascular resistance. Seven newborn piglets were acutely instrumented. A transit-time ultrasound flow probe was placed around the renal artery and a femoral arterial catheter was placed for blood pressure monitoring. Epinephrine was infused in doubling doses from 0.2 to 3.2 μg∙kg−1∙min−1. Mean arterial blood pressure increased from 54 mmHg (1 mmHg = 133.3 Pa) to an average of 96 mmHg at 3.2 μg∙kg−1∙min−1 of epinephrine. Renal blood flow increased from 165 mL∙min−1∙100 g−1 at baseline to 185 mL∙min−1∙100 g−1 at a dose of 0.2 μg∙kg−1∙min−1 and increased further at 0.4 and 0.8 μg∙kg−1∙min−1 to reach 261 mL∙min−1∙100 g−1. Renal blood flow began to fall at a dose of 3.2 μg∙kg−1∙min−1, remaining however, significantly above baseline (211 mL∙min−1∙100 g−1). Consequently, calculated renal vascular resistance fell as the dose was increased from 0.2 to 0.8 μg∙kg−1∙min−1 and then rose again at 1.6 and 3.2 μg∙kg−1∙min−1, being significantly above baseline at 3.2 μg∙kg−1∙min−1. These results demonstrate that epinephrine when given by systemic infusion to the halothane-anesthetized newborn pig is a renal vasodilator at low doses and causes renal vasoconstriction at moderate to high doses. Renal blood flow remained above baseline at all doses tested, and thus, within the dosage range tested, epinephrine infusion should not cause renal ischemia.Key words: epinephrine, kidney blood flow, piglet, renal vascular resistance.

Sign in / Sign up

Export Citation Format

Share Document