title: Vascular smooth muscle responses in normo- and hypertensive rats to sympathetic nerve stimulation and putative transmitters.
abstract: 1. Using changes in perfusion pressure as a measure of end organ response, the effects of field stimulation (0.5 ms supramaximal voltage), noradrenaline (NA, 10(-5)-10(-3) M), adrenaline (ADR, 10(-6)-10(-4) M) and adenosine triphosphate (ATP, 10(-4)-10(-2) M) on the tail artery and mesenteric bed preparations in both normotensive (WKY) and spontaneously hypertensive (SHR) rats were examined. 2. The pressor responses in both preparations from SHR rats to field stimulation, NA and ADR were significantly (P less than 0.05) greater than those from age-matched WKY controls. Responses of both preparations to ATP in normo- and hypertensive rats did not differ significantly. 3. In both preparations from either WKY or SHR rats, pressor responses to ATP (10(-4)-10(-2) M) were inhibited by alpha,beta-methylene ATP (alpha,beta MeATP, 1 x 10(-6) M) while those to field stimulation were not. Phentolamine (2 x 10(-6) M) and prazosin (1 x 10(-7) M) each inhibited the pressor responses to both field stimulation, NA and ADR. 4. [3H] was released by field stimulation from tail arteries pre-incubated with either [3H]-NA or [3H]-adenosine in both normotensive and hypertensive rats. Release in each case was abolished by tetrodotoxin (1 x 10(-6) M). 5. There was no significant difference in the stimulation-evoked [3H]-NA overflow between SHR & WKY rats, alpha,beta MeATP had no significant inhibitory effect on the overflow of [3H] following incubation with [3H]-NA from either group of animals. 6. In the presence of diltiazem (2 x 10(-6) M) and prazosin (5 x 10(-7) M) to abolish any squeezing effect of muscle contractions on ATP release, there was no significant difference in the [3H] overflow between tail arteries from SHR and WKY rats following incubation with [3H]-adenosine. 7. The results confirm the increased response to nerve stimulation in hypertensive animals, an effect probably mediated postsynaptically via alpha-adrenoreceptors. There was no evidence for the involvement of ATP in the hypertensive state.
authors.affiliation: Department of Pharmacology, University of Glasgow, UK.
authors.forename: T C
authors.initials: TC
authors.lastname: Muir
authors.forename: K A
authors.initials: KA
authors.lastname: Wardle
mesh_terms: D000255:Adenosine Triphosphate / Q000502:physiology; D000818:Animals; D004110:Diltiazem / Q000494:pharmacology; D004558:Electric Stimulation; D004837:Epinephrine / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000502:physiology; D011224:Prazosin / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013564:Sympathetic Nervous System / Q000502:physiology*
chemical_list: D000255:Adenosine Triphosphate; D004110:Diltiazem; D009638:Norepinephrine; D011224:Prazosin; D004837:Epinephrine