Abstract
To determine the contribution of nitric oxide (NO) to the vasodilator response induced by salbutamol in diaphragmatic microcirculation, we studied a diaphragmatic preparation in anesthetized rats. With bicarbonate buffered Ringer solution continuously suffusing the diaphragm, laser-Doppler flowmetry was used to record micro vascular blood flow (Q(LDF)). The drugs were applied to the surface of the diaphragm. Salbutamol (3.2 x 10-7-10-4 M), isoproterenol (3.2 x 10-8-3.2 x 10-6 M), and forskolin (3.2 x 10-7- 10-5 M) each elicited a concentration-dependent increase in Q(LDF). The vasodilator response induced by salbutamol (3.2 x 10-7, 10-6, and 3.2 x 10-6 M) was attenuated by a 15-min suffusion of N(w)-nitro-L-arginine (L- NNA, 10-4 M), and pretreatment with L-arginine (10-2 M) could restore salbutamol-induced vasodilator responses. Salbutamol-induced vasodilation was also abolished by propranolol (10-5 M). Similarly, the vasodilator response elicited by isoproterenol (3.2 x 10-8, 10-7, and 3.2 x 10-7 M) and forskolin (3.2 x 10-7, 10-6, and 3.2 x 10-6 M) was inhibited by L-NNA (10-4 M). In contrast, the vasodilator response induced by adenosine (10- 6, 10-5, and 10-4 M) was not affected by L-NNA (10-4 M). These data indicate that in rat diaphragmatic microcirculation salbutamol-induced vasodilation may be partly mediated by β-adrenoceptors on the endothelium. Moreover, these data suggest that an elevation of cyclic AMP in the endothelium may cause release of NO.
| Original language | English |
|---|---|
| Pages (from-to) | H2173-H2179 |
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 272 |
| Issue number | 5 41-5 |
| DOIs | |
| Publication status | Published - 1997 |
All Science Journal Classification (ASJC) codes
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)