The role of coronary adrenergic receptors in the response to nitroglycerine and the regulation of large and small vessel resistance.

Autor: Malindzak GS Jr, Kosinski EJ, Green HD, Yarborough GW
Jazyk: angličtina
Zdroj: Archives internationales de pharmacodynamie et de therapie [Arch Int Pharmacodyn Ther] 1978 Oct; Vol. 235 (2), pp. 299-316.
Abstrakt: The role of coronary adrenergic receptors in response to nitroglycerine and in the regulation of large and small coronary vascular resistance was evaluated in two separate studies involving fifteen anesthetized mongrel dog preparations, before and after alpha- and beta-adrenergic blockade, respectively. Coronary blood flow (CBF) was measured through the left anterior descending (LAD) coronary artery by a non-cannulating electromagnetic flow probe. Pressure catheters were inserted into the arch of the aorta and into a distal apical branch of the LAD coronary artery to measure, respectively, aortic pressure (coronary perfusion pressure (PA), peripheral coronary pressure )PC), and coronary artery pressure gradient (PG = PA -PC). End-diastolic resistances to flow were computed as: (a) large coronary end-diastolic resistance (RL = PG/CBF), and (B) small coronary end-diastolic resistance (RS = PC/CBF). Nitroglycerine (NG) alone increased RL to approximately 180--220% of control and reduced RS to about 60% of control, respectively. Following pharmacologic blockade with propranolol (PRO), NG increased RL to about 180% of control and reduced RS to about 60% of control. Following alpha blockade with phenoxybenzamine (PBZ), NG decreased RL to about 78% of control and decreased RS to about 56% of control. It is concluded that while the overall effect of NG on the coronary vascular resistance is one of vasodilation, RL appears to be increased transiently and RS transiently decreased. Alpha adrenergic blockade appears to abolish this response. The increase in RL in response to NG appears to be associated with the systemic hypotensive effect in response to NG. It is proposed that the observed increase in RL is produced by the increase in cardiac sympathetic nerve activity which is initiated by the systemic hypotensive effect of NG.
Databáze: MEDLINE