Methyclothiazide (0.1 mM) reduces Ca2+ contractures with maximal inhibition of 90.4% in SHR aortic rings with endothelium. The inhibitory effect of Methyclothiazide (0.1 mM) on Ca2+ contracture is significantly but not totally abolished by the NO synthase inhibitor in SHR aortic rings with functional endothelium. [1] Methyclothiazide (0.1 mM) induces endothelium-dependent inhibition of the vasoconstrictor responses to NE and AVP only in aortas from spontaneously hypertensive rats (SHR) rather than normotensive Wistar Kyoto rats (WKY), and the maximal vasoconstrictive effect of NE and AVP is decreased by 59% and 32.3%, respectively. [2] Methyclothiazide (3.5 mM) inhibits renin release in rat kidney slices. [3]

Methyclothiazide (0.1 g/L for the first 5 weeks and 0.2 g/L for the second 2 weeks, drinking water) attenuates development of hypertension in salt-sensitive (DS) rats, but does not affect blood pressure in salt-resistant (DR) ones. [4] The methyclothiazide-treated DOCA-salt rats weigh less than controls or the nonsupplemented DOCA-salt rats at weeks 3 and 4. Methyclothiazide added to the drinking water of DOCA-salt rats attenuates the elevation of blood pressure. [5]