Adrenergic Potentiation by Angiotensin II in Isolated Canine Cutaneous Arteries: Effect of Bathing Media and Calcium

Povolny, Kathleen M.; Jung, Richard W.; Kraft, E; Zimmerman, Ben G.

doi:10.1159/000158118

Cited by 8 publications

(9 citation statements)

References 10 publications

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“…[16][17][18][19][20][21]. In this study, we report on one mecha nism whereby angiotensin II increases the sensitivity of arteries to norepinephrine and clonidine.…”

Section: Discussionmentioning

confidence: 99%

Protein Kinase C as a Modulator of Response Amplification in Vascular Smooth Muscle

Laher

Thompson²,

Gagne³

1990

J Vasc Res

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The amplification of α-adrenoceptor-mediated vasoconstriction by angiotensin II was studied in femoral artery rings from rabbits. Threshold concentrations of angiotensin II (0.1 nM) increased the maximal response to clonidine to 139 ± 8% of control and produced a 3.2-fold increase in sensitivity. These effects of angiotensin II were reversed when tissues were pretreated with staurosporine (50 nM), an inhibitor of protein kinase C. The amplification of the α-adrenoceptor-mediated vasoconstrictor effects of thrombin and norepinephrine by angiotensin II were also reversed by pretreatment with staurosporine. Angiotensin II induced a response amplification in vascular smooth muscle known to be a nonspecific phenomenon, implying postreceptor interaction at intracellular transducer systems. Our findings suggest that upon activation of protein kinase C by angiotensin II, arterial responses to α-adrenoceptor agonists are amplified. This provides for nonspecific changes in vascular sensitivity by tonic alterations in postsynaptic modulation by enzyme systems known to regulate Ca²⁺-dependent phenomena, e.g. those related to vascular excitation-contraction mechanisms.

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“…[16][17][18][19][20][21]. In this study, we report on one mecha nism whereby angiotensin II increases the sensitivity of arteries to norepinephrine and clonidine.…”

Section: Discussionmentioning

confidence: 99%

Protein Kinase C as a Modulator of Response Amplification in Vascular Smooth Muscle

Laher

Thompson²,

Gagne³

1990

J Vasc Res

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“…Tris is frequently used as a buffering system for physiological saline solution and has also been reported to have some adverse effects on smooth muscle contraction (9,10,22,30). In the present experiments, the effects of Tris-buffered solution on the K+-induced re laxation in rat aortic smooth muscle were examined and compared with those of bi carbonate (BC)-buffered solution or N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered solution.…”

Section: Introductionmentioning

confidence: 99%

Effect of Transmembrane pH Gradient Changes on Potassium-Induced Relaxation in Vascular Smooth Muscle

Karaki¹,

Weiss²

1981

J Vasc Res

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In bicarbonate-buffered solution the Ba⁺⁺-induced contraction of rat aorta was relaxed by an elevated extracellular K⁺ concentration. When the pH of the bicarbonate-buffered solution was lowered or the buffer system of the solution changed from bicarbonate to Tris or HEPES, the K⁺-induced relaxation was strongly inhibited. Raising the pH of the Tris-buffered solution restored the effect of K⁺. Addition of NH⁺₄, which is known to cause a transient increase in intracellular pH, transiently inhibited and subsequently augmented the K⁺-induced vasodilation in all solutions. It is suggested that the K⁺-induced vasodilation results from membrane hyperpolarization following enhanced Na⁺, K⁺-ATPase activity and that this K⁺-induced vasodilation is affected by changes in the transmembrane pH gradient.

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“…In this case, other mediators of vascular tone may interact with the ability of the sympathetic nervous system to regulate renal function. The vasoconstrictor responses to adrenergic nerve stimulation have been shown to be augmented by ANG II (11), and ANG II affects transmission at the nerve terminals (15). The response of the blood vessels to norepinephrine may also be potentiated by ANG II (16).…”

mentioning

confidence: 99%

Is the chronically denervated kidney supersensitive to catecholamines?

Ramchandra

Barrett

Guild

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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One method for discerning the role of the renal sympathetic nerves in the regulation of renal function has been to chronically denervate one kidney. One concern with this approach is that increased renal responsiveness to plasma levels of norepinephrine may develop over time. This may reduce the apparent magnitude of the effect of the renal nerves or indeed completely mask their effect. In the present experiment, we used the rabbit unilateral denervated kidney model to examine the acute renal blood flow responses to phenylephrine to determine if there were differences between the responses in chronically denervated kidneys compared with either intact or acutely denervated kidneys. In addition, we examined the responses in rabbits that had been made hypertensive using a continuous infusion of ANG II for 7 wk. We found that chronic denervation did not result in increased renal responsiveness to phenylephrine compared with either the intact or acutely denervated kidney, suggesting that differences in renal function between renal nerve-intact and -denervated kidneys observed in previous studies are unlikely to be confounded by supersensitivity. These results suggest that the unilateral denervated kidney model is a valid model to study the role of the renal nerves in the regulation of renal function.

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Adrenergic Potentiation by Angiotensin II in Isolated Canine Cutaneous Arteries: Effect of Bathing Media and Calcium

Cited by 8 publications

References 10 publications

Protein Kinase C as a Modulator of Response Amplification in Vascular Smooth Muscle

Protein Kinase C as a Modulator of Response Amplification in Vascular Smooth Muscle

Effect of Transmembrane pH Gradient Changes on Potassium-Induced Relaxation in Vascular Smooth Muscle

Is the chronically denervated kidney supersensitive to catecholamines?

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