The influence of H1- and H2-receptor blockade on responses of resistance and capacitance vessels to noradrenaline in working skeletal muscles in cats

Janczewska, H; Maśliński, S

doi:10.1007/bf01991478

Cited by 2 publications

(1 citation statement)

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“…However, oral administration of indomethacin may have minimized the drug's effectiveness, since intravenous injection of indomethacin has been shown to augment vascular resistance in dynamically contracting dog skeletal muscle. 34 Consequently, it appears that vascular resistance and, in turn, blood flow in exercising muscle can be reduced after indomethacin, a situation that would favor an enhanced build-up of substances capable of inducing the exercise reflex. This would suggest that the vasodilator action of protaglandins is important during dynamic exercise.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandins contribute to cardiovascular reflexes evoked by static muscular contraction.

Stebbins¹,

Maruoka

Longhurst

1986

Circulation Research

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The purpose of this study was to determine the contribution of prostaglandins to the reflex cardiovascular responses induced by static contraction of the hind limb in cats, i.e., the exercise reflex. To accomplish this, the cardiovascular responses to hind limb contraction induced by electrical stimulation of spinal cord ventral roots L^ and S, were compared before and after inhibition of prostaglandin synthesis (indomethacin, 2-6 mg/kg i.v., n = 5, or sodium meclofenamate, 2-6 mg/kg i.v., n = 5) or after injection of prostaglandin E 2 into the hind limb arterial blood supply. Treatment with indomethacin attenuated the contraction-induced increase in mean arterial pressure and left ventricular dP/dt by 76% and 86%, respectively. Heart rate and average developed triceps surae muscle tension were unchanged. After administering sodium meclofenamate, the reflex response was attenuated to a similar degree. In the indomethacin-treated animals, injection of exogenous prostaglandin E 2 (PGE 2 ) partially restored the pressor and myocardial contractile responses. In 6 animals, treatment with exogenous PGE 2 without prior inhibition of prostaglandin synthesis did not significantly augment the contraction-induced cardiovascular response. Using the radioactive microsphere technique, we measured skeletal muscle blood flow during contraction before and after treatment with indomethacin (n = 6) to determine if an indomethacin-induced alteration in blood flow could account for the attenuated contraction-induced cardiovascular response. Blood flow during static muscle contraction was not significantly altered by indomethacin. We conclude that prostaglandins contribute to the exercise reflex through an action on afferent nerve endings rather than through a regional vascular effect. (Circulation Research 1986;59:645-654)

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Section: Discussionmentioning

confidence: 99%