Bradykinin-induced vasoconstriction of rat mesenteric arteries precontracted with noradrenaline.

1. Administration of bradykinin caused dose-dependent vasoconstriction in rat isolated perfused mesenteric arteries precontracted with noradrenaline. 2.

Organic and inorganic calcium blockers on voltage and receptor operated channels of resistance arteries of the rat.

The vasoconstrictor responses induced by noradrenaline (NA), adrenaline (AD), serotonin (ST) and vasopressin (VP) on the anterior mesenteric artery of the rat and its branches, were maintained, although somewhat reduced when perfused with a Ca free solution that depletes extracellular Ca. The vasoconstrictor responses were abolished when Lanthanum, EDTA, Verapamil or Nifedipine were added to the Ca free solution. These drugs are known to displace plasmalemmal bound Ca that triggers vasoconstriction when the agonists attach to the receptors thus blocking the vasoconstrictor responses.

Calcium pools in the contraction of arterial smooth muscle induced by several agonists.

After perfusing the vascular circuit of the mesenteric artery of the rat with a Ca-free solution for 20 min, extracellular Ca was depleted, and the vasoconstrictor effect of high K solutions was abolished, while the vasopressin response was reduced by 40%, serotonin by 30% and noradrenaline and adrenaline responses by about 20%. When the Ca-free perfusion was prolonged for 2 h or more, the vascular responses to the agonists were further reduced due to depletion of cellular Ca. Successive doses of each agonist injected at 1 min intervals showed a decline of the responses, that recovered when 4 min or more were allowed to pass after the last injection.

Angiotensin I, II, and II tachyphylaxis in the mesenteric vascular circuit of the rat.

Angiotensin tachyphylaxis is rapidly induced in the mesenteric vascular circuit of the rat perfused with a saline solution. there is crossed tachyphylaxis among angiotensins (AI, AII, and AIII). The angiotensin antagonist Sar 1-Ileu 8-AII is ineffective when the vascular preparation is previously rendered tachyphylactic to AII, showing that the AII receptors are not available during tachyphylaxis.

The effect of thyroid hormone on renin production and release by rat kidney slices.

The effect of thyroid hormone on renin productiona and release by rat kidney slices was studied. Rat kidney slices were incubated in Warburg flasks containing Krebs-Ringer-Phosphate- Glucose- Dextran solution at 37 C for 5 hours. Renin content, renin released into the incubation media and oxygen consumption were measured.