Received January 15, 2004
Revised February 3, 2004
Accepted after revision February 26, 2004

¹ University of Buenos Aires

^* To whom correspondence should be addressed. E-mail: afellet{at}huemul.ffyb.uba.ar.

	Abstract

We previously reported that acute NG-nitro-L-arginine methyl ester (L-NAME) administration increases mean arterial pressure (MAP) and heart rate (HR) in autonomic blocked (CAB) anesthetized rats. The present study examined whether thyroid and adrenal glands are involved in these pressor and chronotropic responses. Sprague-Dawley rats were studied after bilateral vagotomy and ganglionic blockade with hexamethonium (10 mg k (-1)), stabilizing MAP with a phenylephrine (PE) infusion (6 µg k(-1) min (-1)). Groups of rats: L: CAB; PE: CAB+PE bolus (6 µg k (-1)); L-TX: thyroidectomy+CAB; L-AX: adrenalectomy+CAB; TX: only thyroidectomy. L, L-AX and L-TX groups received a bolus of L-NAME (7.5 mg k (-1)). Triiodothyronine (T3), thyroxin (T4) and thyrotropin (TSH) levels were measured in L and L-TX groups before and after L-NAME bolus. NADPH diaphorase activity was determined in heart and aorta of TX group. The pressor response induced by L-NAME was similar in all groups. L-NAME induced-tachycardia was associated with this rise in MAP. Adrenalectomy did not modify this chronotropic response, but it was attenuated by thyroidectomy. Thyroidectomy by itself decreased the circulating levels of T3 but it had no effect on the plasmatic levels of T4 and TSH. L and L-TX groups showed similar levels of circulating T4 and TSH, meanwhile plasmatic level of T3 decreased in L group. NOS activity in atria as well as in aorta was greater in TX group compared with control rats. Thyroid gland modulates intrinsic heart rate throughout a mechanism that involves, at least in part, nitric oxide pathway in a heart without autonomic influences.

Key Words: Cardiovascular, Nitric oxide, Thyroid hormone