scholarly journals p66Shc regulates renal vascular tone in hypertension-induced nephropathy

2016 ◽  
Vol 126 (7) ◽  
pp. 2533-2546 ◽  
Author(s):  
Bradley Miller ◽  
Oleg Palygin ◽  
Victoriya A. Rufanova ◽  
Andrew Chong ◽  
Jozef Lazar ◽  
...  
Keyword(s):  
Vascular Tone ◽  
Renal Vascular ◽  
Renal Vascular Tone

Stimulation of renin release by prostaglandin E2 is mediated by EP2 and EP4 receptors in mouse kidneys

2004 ◽  
Vol 287 (3) ◽  
pp. F427-F433 ◽  
Author(s):  
Frank Schweda ◽  
Jürgen Klar ◽  
Shuh Narumiya ◽  
Rolf M. Nüsing ◽  
Armin Kurtz
Keyword(s):  
Vascular Tone ◽  
Threshold Concentration ◽  
Renin Release ◽  
Receptor Subtypes ◽  
Wild Type ◽  
Adrenoceptor Agonist ◽  
Functional Relevance ◽  
Renal Vascular ◽  
Renal Vascular Tone ◽  
Stimulation Of

PGE2 is a potent stimulator of renin release. So far, the contribution of each of the four PGE2 receptor subtypes (EP1–EP4) in the regulation of renin release has not been characterized. Therefore, we investigated the effects PGE2 on renin secretion rates (RSR) from isolated, perfused kidneys of EP1−/−, EP2−/−, EP3−/−, EP4−/−, and wild-type mice. PGE2 concentration dependently stimulated RSR from kidneys of all four knockout strains with a threshold concentration of 1 nM in EP1−/−, EP2−/−, EP3−/−, and wild-type mice, whereas the threshold concentration was shifted to 10 nM in EP4−/− mice. Moreover, the maximum stimulation of RSR by PGE2 at 1 μM was significantly reduced in EP4−/− (12.8-fold of control) and EP2−/− (15.9-fold) compared with wild-type (20.7-fold), EP1−/− (23.8-fold), and EP3−/− (20.1-fold). In contrast, stimulation of RSR by either the loop diuretic bumetanide or the β-adrenoceptor agonist isoproterenol was similar in all strains. PGE2 exerted a dual effect on renal vascular tone, inducing vasodilatation at low concentrations (1 nmol/) and vasoconstriction at higher concentrations (100 nmol/) in kidneys of wild-type mice. In kidneys of EP2−/− as well as EP4−/− mice, vasodilatation at low PGE2 concentrations was prevented, whereas vasoconstriction at higher concentrations was augmented. In contrast, the vasodilatatory component was pronounced in kidneys of EP1 and EP3 knockout mice, whereas in both genotypes the vasoconstriction at higher PGE2 concentrations was markedly blunted. Our data provide evidence that PGE2 stimulates renin release via activation of EP2 and EP4 receptors, whereas EP1 and EP3 receptors appear to be without functional relevance in juxtaglomerular cells. In contrast, all four receptor subtypes are involved in the control of renal vascular tone, EP1 and EP3 receptors increasing, and EP2 as well as EP4 receptors, decreasing it.

Effect of Captopril on Renal Vascular Tone in Patients with Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 421s-423s ◽  
Author(s):  
A. Mimran ◽  
H. R. Brunner ◽  
G. A. Turini ◽  
B. Waeber ◽  
D. Brunner
Keyword(s):  
Essential Hypertension ◽  
Vascular Tone ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Urinary Potassium ◽  
Renal Vascular ◽  
Renal Vascular Tone

1. The effect of acute inhibition of angiotensin-converting enzyme by captopril (50 mg) on renal haemodynamics and function was assessed in nine patients with essential hypertension on unrestricted sodium intake (n = 8) or low sodium diet (n = 1). 2. Captopril induced a rapid and significant decrease in arterial pressure, which was maximal within 60 min. 3. Effective renal plasma flow (ERPF) increased, glomerular filtration rate (GFR) did not change and filtration fraction (FF) decreased after captopril. No change in sodium excretion and a decrease in urinary potassium occurred. 4. In the patient on low sodium diet, captopril induced striking increases in GFR and ERPF (64 and 106% respectively). 5. The logarithm of baseline plasma renin activity was positively correlated with the change in ERPF and negatively correlated with changes in FF and renal resistance. 6. The results indicate that in patients with essential hypertension angiotensin participates actvely in the maintenance of renal vascular tone at the efferent arteriolar level. A possible influence of kinins remains to be defined.

Interactions Between Neural and Hormonal Mediators of Renal Vascular Tone in Anaesthetized Rabbits

2003 ◽  
Vol 88 (2) ◽  
pp. 229-241 ◽  
Author(s):  
Sarah-Jane Guild ◽  
Carolyn J. Barrett ◽  
Roger G. Evans ◽  
Simon C. Malpas
Keyword(s):  
Vascular Tone ◽  
Renal Vascular ◽  
Renal Vascular Tone

Contribution of endothelin to renal vascular tone and autoregulation in the conscious dog

1999 ◽  
Vol 276 (3) ◽  
pp. F417-F424 ◽  
Author(s):  
Heike Berthold ◽  
Klaus Münter ◽  
Armin Just ◽  
Hartmut R. Kirchheim ◽  
Heimo Ehmke
Keyword(s):  
Time Course ◽  
Vascular Tone ◽  
Ace Inhibition ◽  
Renal Hemodynamics ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Renal Autoregulation ◽  
Arterial Blood ◽  
Renal Vascular ◽  
Renal Vascular Tone

Exogenous endothelin-1 (ET-1) is a strong vasoconstrictor in the canine kidney and causes a decrease in renal blood flow (RBF) by stimulating the ETA receptor subtype. The aim of the present study was to investigate the role of endogenously generated ET-1 in renal hemodynamics under physiological conditions. In six conscious foxhounds, the time course of the effects of the selective ETA receptor antagonist LU-135252 (10 mg/kg iv) on mean arterial blood pressure (MAP), heart rate (HR), RBF, and glomerular filtration rate (GFR), as well as its effects on renal autoregulation, were examined. LU-135252 increased RBF by 20% (from 270 ± 21 to 323 ± 41 ml/min, P < 0.05) and HR from 76 ± 5 to 97 ± 8 beats/min ( P< 0.05), but did not alter MAP, GFR, or autoregulation of RBF and GFR. Since a number of interactions between ET-1 and the renin-angiotensin system have been reported previously, experiments were repeated during angiotensin converting enzyme (ACE) inhibition by trandolaprilat (2 mg/kg iv). When ETA receptor blockade was combined with ACE inhibition, which by itself had no effects on renal hemodynamics, marked changes were observed: MAP decreased from 91 ± 4 to 80 ± 5 mmHg ( P < 0.05), HR increased from 85 ± 5 to 102 ± 11 beats/min ( P < 0.05), and RBF increased from 278 ± 23 to 412 ± 45 ml/min ( P< 0.05). Despite a pronounced decrease in renal vascular resistance over the entire pressure range investigated (40–100 mmHg), the capacity of the kidneys to autoregulate RBF was not impaired. The GFR remained completely unaffected at all pressure levels. These results demonstrate that endogenously generated ET-1 contributes significantly to renal vascular tone but does not interfere with the mechanisms of renal autoregulation. If ETAreceptors are blocked, then the vasoconstrictor effects of ET-1 in the kidney are compensated for to a large extent by an augmented influence of ANG II. Thus ET-1 and ANG II appear to constitute a major interrelated vasoconstrictor system in the control of RBF.

Physiological and pathophysiological roles of oxygen radicals in the renal microvasculature

2002 ◽  
Vol 282 (2) ◽  
pp. R335-R342 ◽  
Author(s):  
Christine G. Schnackenberg
Keyword(s):  
Diabetes Mellitus ◽  
Oxygen Radicals ◽  
Vascular Tone ◽  
Tubuloglomerular Feedback ◽  
Normal Kidney ◽  
Renal Vasoconstriction ◽  
Increased Sensitivity ◽  
Renal Microvasculature ◽  
Renal Vascular ◽  
Renal Vascular Tone

The renal microvasculature is an important component in the regulation of kidney function. Recent studies suggest that oxygen radicals can contribute to the modulation of renal cortical and medullary microvascular function under normal conditions as well as in pathophysiological conditions such as diabetes mellitus and hypertension. This review focuses on studies that indicate oxygen radicals can cause renal vasoconstriction, mediate the vasoconstriction of other agonists, and modulate nitric oxide-dependent actions in the normal kidney. Hypertension and diabetes mellitus are associated with oxidative stress. Recent investigations suggest that oxygen radicals may contribute to the enhanced renal vascular tone, increased sensitivity to vasoconstrictors, impaired endothelium-dependent vasodilation, and enhanced tubuloglomerular feedback found in these pathophysiological conditions.

Renovascular BKCa channels are not activated in vivo under resting conditions and during agonist stimulation

2007 ◽  
Vol 292 (1) ◽  
pp. R345-R353 ◽  
Author(s):  
Linda Magnusson ◽  
Charlotte Mehlin Sorensen ◽  
Thomas Hartig Braunstein ◽  
Niels-Henrik Holstein-Rathlou ◽  
Max Salomonsson
Keyword(s):  
Vascular Tone ◽  
Ang Ii ◽  
Small Reduction ◽  
Bkca Channels ◽  
Agonist Stimulation ◽  
Electromagnetic Flowmetry ◽  
Renal Vascular ◽  
Renal Vascular Tone

We investigated the role of large-conductance Ca2+-activated K+ (BKCa) channels for the basal renal vascular tone in vivo. Furthermore, the possible buffering by BKCa of the vasoconstriction elicited by angiotensin II (ANG II) or norepinephrine (NE) was investigated. The possible activation of renal vascular BKCa channels by cAMP was investigated by infusing forskolin. Renal blood flow (RBF) was measured in vivo using electromagnetic flowmetry or ultrasonic Doppler. Renal preinfusion of tetraethylammonium (TEA; 3.0 μmol/min) caused a small reduction of baseline RBF, but iberiotoxin (IBT; 0.3 nmol/min) did not have any effect. Renal injection of ANG II (1–4 ng) or NE (10–40 ng) produced a transient decrease in RBF. These responses were not affected by preinfusion of TEA or IBT. Renal infusion of the BKCa opener NS-1619 (90.0 nmol/min) did not affect basal RBF or the response to NE, but it attenuated the response to ANG II. Coadministration of NS-1619 with TEA or IBT abolished this effect. Forskolin caused renal vasodilation that was not inhibited by IBT. The presence of BKCa channels in the preglomerular vessels was confirmed by immunohistochemistry. Despite their presence, there is no indication for a major role for BKCa channels in the control of basal renal tone in vivo. Furthermore, BKCa channels do not have a buffering effect on the rat renal vascular responses to ANG II and NE. The fact that NS-1619 attenuates the ANG II response indicates that the renal vascular BKCa channels can be activated under certain conditions.

scholarly journals Vestibular stimulation leads to distinct hemodynamic patterning

2000 ◽  
Vol 279 (1) ◽  
pp. R118-R125 ◽  
Author(s):  
I. A. Kerman ◽  
B. A. Emanuel ◽  
B. J. Yates
Keyword(s):  
Vascular Tone ◽  
Systemic Blood Pressure ◽  
Vestibular Stimulation ◽  
Doppler Flowmetry ◽  
Afferent Activation ◽  
Pressor Responses ◽  
Renal Vascular ◽  
Vestibulosympathetic Reflexes ◽  
Renal Vascular Tone ◽  
Stimulation Of

Previous studies demonstrated that responses of a particular sympathetic nerve to vestibular stimulation depend on the type of tissue the nerve innervates as well as its anatomic location. In the present study, we sought to determine whether such precise patterning of vestibulosympathetic reflexes could lead to specific hemodynamic alterations in response to vestibular afferent activation. We simultaneously measured changes in systemic blood pressure and blood flow (with the use of Doppler flowmetry) to the hindlimb (femoral artery), forelimb (brachial artery), and kidney (renal artery) in chloralose-urethane-anesthetized, baroreceptor-denervated cats. Electrical vestibular stimulation led to depressor responses, 8 ± 2 mmHg (mean ± SE) in magnitude, that were accompanied by decreases in femoral vasoconstriction (23 ± 4% decrease in vascular resistance or 36 ± 7% increase in vascular conductance) and increases in brachial vascular tone (resistance increase of 10 ± 6% and conductance decrease of 11 ± 4%). Relatively small changes (<5%) in renal vascular tone were observed. In contrast, electrical stimulation of muscle and cutaneous afferents produced pressor responses (20 ± 6 mmHg) that were accompanied by vasoconstriction in all three beds. These data suggest that vestibular inputs lead to a complex pattern of cardiovascular changes that is distinct from that which occurs in response to activation of other types of somatic afferents.

RENAL VASCULAR TONE IN ESSENTIAL AND SECONDARY HYPERTENSION

Medicine ◽  
1975 ◽  
Vol 54 (1) ◽  
pp. 29-44 ◽  
Author(s):  
N K HOLLENBERG ◽  
D F ADAMS ◽  
H SOLOMON ◽  
W R CHENITZ ◽  
B M BURGER ◽  
...  
Keyword(s):  
Vascular Tone ◽  
Secondary Hypertension ◽  
Renal Vascular ◽  
Renal Vascular Tone

scholarly journals Doppler resistive index to reflect regulation of renal vascular tone during sepsis and acute kidney injury

Critical Care ◽  
2012 ◽  
Vol 16 (5) ◽  
pp. R165 ◽  
Author(s):  
Antoine Dewitte ◽  
Julien Coquin ◽  
Bertrand Meyssignac ◽  
Olivier Joannès-Boyau ◽  
Catherine Fleureau ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Vascular Tone ◽  
Resistive Index ◽  
Kidney Injury ◽  
Renal Vascular ◽  
Renal Vascular Tone

Induced renal vasomotion in the intact dog

1962 ◽  
Vol 202 (5) ◽  
pp. 888-892 ◽  
Author(s):  
Ignatios J. Voudoukis ◽  
Robert J. Boucek
Keyword(s):  
Vascular Tone ◽  
Control Level ◽  
Renal Arteries ◽  
X Ray ◽  
Before And After ◽  
Extreme Sensitivity ◽  
Long Acting ◽  
Renal Vascular ◽  
Control State ◽  
Renal Vascular Tone

X-ray viewing of the opacified artery at a preselected interval before and after the administration of a pressor substance permits the study of induced vascular motion. This technique applied to the renal arteries of the dog demonstrated their extreme sensitivity to the catecholamines. With certain of these drugs, the effect persisted even after the return of the blood pressure to the control level. Two types of renal vascular responses occurred. One was characterized by an apparent increased resistance in the arteries distal to the third division and followed the administration of short-duration pressor compounds. The second type of response, occurring after the use of long-acting pressor compounds, was more general affecting all sizes of arteries, the divisions of the renal arteries being extraordinarily sensitive. Spinal cord damage, producing paraplegia, apparently reduced the renal vascular tone as the runoff of the radiopaque substance into the kidney was enhanced. This improved the clarity of the arteriograms. The induced vasodilation of the paraplegic animal was returned to the control state by the administration of epinephrine or norepinephrine.

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