Nitric Oxide Mediates Cat Hindlimb Cholinergic Vasodilation Induced by Stimulation of Posterior Hypothalamus.

Abstract

The aim of this work was to examine whether endothelium-derived relaxing factor (nitric oxide) mediates cat hindlimb cholinergic vasodilation induced by stimulation of the posterior hypothalamus and beta-adrenergic vasodilation by I.V. injection of isoproterenol using an inhibitor of nitric oxide synthesis, NW-nitro-L-arginine methyl ester (L-NAME). Without L-NAME, femoral blood flow velocity (FBV) increased during hypothalamic stimulation by 11.2 +/- 2.2 cm/s (mean +/- SEM) from the baseline value of 8.4 +/- 2.2 cm/s and femoral conductance (FC) increased by 0.084 +/- 0.021 cm/s/mmHg from 0.062 +/- 0.016 cm/s/mmHg, which were abolished by atropine (0.5 mg I.A.). Arterial blood pressure (AP) and heart rate (HR) increased during hypothalamic stimulation (15 +/- 8 mmHg and 22 +/- 6 beats/min). When isoproterenol (1-2 micrograms I.V.) was injected, FBV and FC increased 5.1 +/- 0.56 cm/s and 0.048 +/- 0.005 cm/s/mmHg. With L-NAME (20-100 mg I.A.), the rises in AP and HR during hypothalamic stimulation were unchanged but the increases in FBV and FC were significantly blunted to 5.2 +/- 3.7 cm/s and 0.026 +/- 0.021 cm/s/mmHg. In contrast, L-NAME did not affect the responses in FBV and FC during stimulation of beta-adrenergic receptors. The effect of NG-monomethyl-L-arginine (10-30 mg I.A.) was the same as L-NAME. It is suggested that nitric oxide is involved in hindlimb cholinergic vasodilation neurally induced by hypothalamic stimulation but not in beta-adrenergic vasodilation.

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

“…Continuous generation of NO appears to be important in regulating basal vascular resistance in skeletal muscle (Du et al, 1992). Sympathetic cholinergic vasodilatation of skeletal muscle small arteries induced by electrical stimulation of the hypothalamic defense area in anes-PHARMACOLOGY OF NEUROGENIC NO IN BLOOD VESSEL 295 thetized cats (Matsukawa et al, 2002) seems to be mediated by NO (Matsukawa et al, 1993). The reflex vasodilatation in the rat hindlimb produced by electrical stimulation of the superior laryngeal nerve involves the release of newly synthesized NO from NOS-positive postganglionic lumbar sympathetic nerves (Possas and Lewis, 1997).…”

Regulation of Increased Blood Flow (Hyperemia) to Muscles During Exercise: A Hierarchy of Competing Physiological Needs

“…This raises the possibility of acetylcholine from sympathetic nerves causing NO release from adjacent vascular endothelium. Other possibilities include a population of nitroxidergic dilator nerves or the release of NO as a cotransmitter from the sympathetic cholinergic nerves (116,309).…”

Forelimb Vasodilatation Induced by Hypothalamic Stimulation Is Greatly Mediated with Nitric Oxide in Anesthetized Cats

“…Such an endotheliummediated vasodilator mechanism may be involved in the sympathetic cholinergic vasodilatation of blood vessels in skeletal muscle. To examine this hypothesis, we investigated the effect of an inhibitor of nitric oxide synthesis on the increase in femoral blood flow induced by stimulation of the hypothalamic defense area [6]. The increase in femoral blood flow by hypothalamic stimulation was blunted but not eliminated Key words: stimulation of the hypothalamic defense area, sympathetic cholinergic nerve, brachial artery, blood flow velocity, vascular conductance.…”