1             Hoe 140 consistently blocked the vasodepressor action of injected bradykinin, but had no

2 revent the breakdown of bradykinin, a potent vasodepressor agent, and prevent the effects of angioten

3 baroreceptors, with a modest cardiopulmonary vasodepressor effect.

4                                  An isolated vasodepressor form was found in 32 (20%) patients, who h

5 identify one third of patients with isolated vasodepressor form.

6 epted cut-off value for the diagnosis of the vasodepressor form.

7 e inotropic effect on cardiac function and a vasodepressor function in the systemic circulation.

8     NO has previously been implicated in the vasodepressor function of apelin; we found that apelin t

9 ts of candesartan were insurmountable, and a vasodepressor or vasodilator response to AngII was not u

10 ing to the fifth percentile) detected 97% of vasodepressor patients, but was also present in 84% of t

11 es of the renin-angiotensin system and other vasodepressor peptides are intertwined through this enzy

12                            Assessment of the vasodepressor reflex in carotid sinus syndrome is influe

13     When an asystolic pause was induced, the vasodepressor reflex was reassessed after suppression of

14 isease, and in some patients may be due to a vasodepressor reflex.

15 nd the nucleus of the solitary tract (NTS; a vasodepressor region).

16 to the RVLM of hypertensive rats blocked the vasodepressor response to intravenous moxonidine.

17 animals transfected with eNOS, and pulmonary vasodepressor responses to bradykinin and the type V cGM