1. The effect of the hypertensive process on vascular sensitivity to serotonin and methysergide was studied.
2. Isometric contractions were recorded from arteries isolated from spontaneously hypertensive (SHR), Kyoto-Wistar normotensive (WKY), deoxycorticosterone acetate (DOCA)-hypertensive and Sprague-Dawley normotensive rats.
3. Arteries from hypertensive rats (except SHR aorta) were more sensitive (lower ED30) to noradrenaline, serotonin and methysergide relative to those from controls.
4. The magnitude of the leftward shift in ED30 was similar for the three agonists in mesenteric and tail arteries from DOCA rats, whereas the shift in ED30 for serotonin and methylsergide in aortae exceeded that to noradrenaline. In SHR, the shift in ED30 for serotonin and methylsergide in tail and mesenteric arteries was greater than that to noradrenaline; SHR aortae did not differ from WKY aortae.
5. Arteries from hypertensive rats (except SHR aorta) developed a greater maximal contraction to methysergide than those from controls; maximal contractions to noradrenaline and serotonin were either less than or similar to those of controls.
6. The agonistic action of methysergide in DOCA rats paralleled the development of high arterial pressure. Low sodium diet abated the high pressure in DOCA rats and reduced vascular sensitivity to all agonists.
7. These observations support the view that in hypertension there is a generalized increase in vasoconstrictor sensitivity. The major finding is that, in two hypertensive models, there is a uniquely greater increase in vascular responsiveness to the agonistic action of methysergide.