Constrictor and compliance responses of some arteries to nerve or drug stimulation.
1. The magnitude of the maximum constrictor response to nerve stimulation was measured in the saphenous, ear, inferior and superior mesenteric, renal and carotid arteries in the rabbit and corresponding arteries, except the ear and carotid, in the guinea-pig. The responses varied from an average rise of 350 mm Hg in the rabbit saphenous to almost no response in the rabbit carotid. The guinea-pig arteries gave consistently smaller responses than the rabbit. The response magnitude was unrelated to wall thickness or the presence of an active uptake mechanism for noradrenaline. The response did correlate with the density of adrenergic innervation, with the wall thickness to lumen ratio and with the function of the artery and the amount of connective tissue in its wall.2. The magnitude of the maximum constrictor response to noradrenaline and six other agonist drugs, acetylcholine, histamine, 5-HT, KCl, vasopressin and angiotensin II, was compared. In all arteries noradrenaline was the most powerful agonist. The maximum responses to nerve stimulation and to noradrenaline were compared. In the rabbit saphenous and ear arteries this ratio was almost 1, but in arteries such as the rabbit renal it fell below 0.5.3. Artery wall stiffness was measured from the pressure/volume relationship during distension of a closed length of artery. In a relaxed artery two components only were present, an early easily distended phase and a late relatively undistensible phase. Noradrenaline caused a third, early, very stiff phase to appear in the pressure/volume curves. This is probably due to contracted muscle. The increase in stiffness varied from 617% in the rabbit saphenous to 152% in the rabbit carotid. In conducting arteries such as the carotid the change in stiffness was a more sensitive index of noradrenaline action than vaso-constriction.4. During the measurement of wall stiffness stress relaxation was not noticeable in relaxed arteries but was prominent in arteries contracted by noradrenaline. Stress relaxation involved both the changes in wall stiffness and the ability to constrict and was reversible even in the continuing presence of agonist drugs.5. Nerve stimulation, even in arteries where its vasoconstrictor effects were equal to those of noradrenaline, gave only slight increases in artery wall stiffness, suggesting that even in these densely innervated arteries only a small fraction of the muscle is activated by nerve stimulation.
D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D002339:Carotid Arteries / Q000502:physiology; D003238:Connective Tissue; D004558:Electric Stimulation; D006168:Guinea Pigs; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects; D009638:Norepinephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011817:Rabbits; D012701:Serotonin / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology
D014667:Vasopressins; D000804:Angiotensin II; D012701:Serotonin; D011189:Potassium Chloride; D006632:Histamine; D000109:Acetylcholine; D009638:Norepinephrine