Evidence for a role of nitric oxide in hindlimb vasodilation induced by hypothalamic stimulation in anesthetized rats

• Published in: Anais da Academia Brasileira de Ciências 2005-06, Vol.77 (2), p.245-257
• Main Authors: Ferreira-Neto, Marcos L, Possas, Olga S, Lopes, Oswaldo U, Cravo, Sérgio L
• Format: Article
• Language: English
• Subjects: Adjuvants, Anesthesia - pharmacology; Adrenalectomy; Adrenergic alpha-Antagonists - pharmacology; Animals; defense reaction; Electric Stimulation - methods; electrical stimulation; estimulação elétrica; fluxo sangüíneo dos membros posteriores; Hemodynamics - drug effects; Hemodynamics - physiology; Hindlimb - blood supply; hindlimb blood flow; hipotálamo; hypothalamus; Hypothalamus - physiology; Male; Multidisciplinarias (Ciencias Sociales y Humanidades); MULTIDISCIPLINARY SCIENCES; NG-Nitroarginine Methyl Ester - pharmacology; Nitric Oxide - physiology; Pentobarbital - pharmacology; Phentolamine - pharmacology; Rats; Rats, Wistar; reação de defesa; Regional Blood Flow - drug effects; Regional Blood Flow - physiology; Vasodilation - drug effects; Vasodilation - physiology
• ISSN: 0001-3765; 1678-2690; 0001-3765; 1678-2690
• DOI: 10.1590/S0001-37652005000200005

Electrical stimulation of the hypothalamus produces cardiovascular adjustments consisting of hypertension, tachycardia, visceral vasoconstriction and hindlimb vasodilation. Previous studies have demonstrated that hindlimb vasodilation is due a reduction of sympathetic vasoconstrictor tone and to activation of beta2-adrenergic receptors by catecholamine release. However, the existence of a yet unidentified vasodilator mechanism has also been proposed. Recent studies have suggested that nitric oxide (NO) may be involved. The aim of the present study was to investigate the role of NO in the hindquarter vasodilation in response to hypothalamic stimulation. In pentobarbital-anesthetized rats hypothalamic stimulation (100 Hz, 150 microA, 6 s) produced hypertension, tachycardia, hindquarter vasodilation and mesenteric vasoconstriction. Alpha-adrenoceptor blockade with phentolamine (1.5 mg/kg, iv) plus bilateral adrenalectomy did not modify hypertension, tachycardia or mesenteric vasoconstriction induced by hypothalamic stimulation. Hindquarter vasodilation was strongly reduced but not abolished. The remaining vasodilation was completely abolished after iv injection of the NOS inhibitor L-NAME (20 mg/kg, iv). To properly evaluate the role of the mechanism of NO in hindquarter vasodilation, in a second group of animals L-NAME was administered before alpha-adrenoceptor blockade plus adrenalectomy. L-NAME treatment strongly reduced hindquarter vasodilation in magnitude and duration. These results suggest that NO is involved in the hindquarter vasodilation produced by hypothalamic stimulation.