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  • aldosterone  (2)
  • Baroreceptor and cardiopulmonary reflexes  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Role of various vasodepressor systems in the acute hypotensive effect of captopril in man (1981)
    Springer
    European journal of clinical pharmacology 20 (1981), S. 1-8 
    Details
    ISSN: 1432-1041
    Keywords: hypertension ; captopril ; angiotensin ; renin ; aldosterone ; catecholamines ; prostaglandins ; kininase II ; hypotensive action
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The acute hypotensive effect of captopril 25 mg was investigated in 26 hypertensive patients (11 with essential and 15 with renal arterial disease). Intra-arterial blood pressure was recorded continuously and arterial blood was sampled for renin, angiotensin I and II, aldosterone, kininase II, catecholamines and prostaglandins. Captopril led to an increase in plasma renin activity, active and total plasma renin concentration and angiotensin I, a decrease in plasma kininase II activity, angiotensin II, aldosterone, prostaglandins E2 and F2* and no change in plasma (nor)adrenaline, dopamine and inactive renin concentration. The hypotensive effect of captopril was related to the changes in plasma angiotensin II level and inversely to the change in prostaglandin E2; the correlation coefficients were low, respectively 0.61 and −0.44. It is likely that the acute hypotensive effect of captopril to some extent is related to changes in plasma angiotensin II and in prostaglandins E2 and F2*. There is no evidence for a role of the adrenergic systems in the hypotensive response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00554659
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  • 2
    Electronic Resource
    Electronic Resource
    Acute haemodynamic and humoral responses to felodipine and metoprolol in mild hypertension (1987)
    Springer
    European journal of clinical pharmacology 32 (1987), S. 71-75 
    Details
    ISSN: 1432-1041
    Keywords: felodipine ; metoprolol ; hypertension ; aldosterone ; angiotensin ; cardiac output ; catecholamines ; pulmonary vascular resistance ; renin ; systemic vascular resistance ; haemodynamic effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Oral administration of felodipine to 10 patients with mild essential hypertension acutely reduced systemic vascular resistance (SVR) by 40% after 30 min. The change in SVR was significantly related to age (r=−0.74). The reduction in the intraarterially measured brachial artery pressure was limited to 15/13 mmHg, due to a rise in cardiac output (CO). The tachycardia was sustained for 90 min, as was an elevation of plasma noradrenaline. There was a transient increase in stroke volume, associated with a reduction in pulmonary capillary wedge pressure, which was at least partly due to a reduced intravascular volume. In contrast to SVR, pulmonary vascular resistance was not affected by felodipine. Addition of intravascular metoprolol after 90 min decreased HR and CO and augmented SVR. The felodipine-induced rise in plasma renin activity (PRA) of 100% was completely reversed by metoprolol. Plasma angiotensin II (PA II) rose by 15% during felodipine, whereas plasma aldosterone concentration (PAC) was not affected. Thus, actuely administered felodipine was a potent dilator of systemic but not of pulmonary arterioles, it stimulated the sympathetic nervous system, and reduced left ventricular filling pressure. The rise in plasma renin did not result in a higher plasma aldosterone level, due partly to reduced generation of angiotensin II.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00609960
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of baroceptor and cardiopulmonary reflexes on neural control of heart rate in normal man, as assessed by power spectral analysis (1992)
    Springer
    Clinical autonomic research 2 (1992), S. 367-371 
    Details
    ISSN: 1619-1560
    Keywords: Baroreceptor and cardiopulmonary reflexes ; Heart rate ; Neurally mediated effect
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study was designed to establish the neurally-mediated effects of baroceptor and cardiopulmonary reflexes on heart rate in normal subjects. We therefore studied the effects of various interventions, able to modify the activity of arterial baroreceptors and cardiopulmonary receptors, on the power spectrum of the R—R interval in nine healthy men. To confirm the efficacy of these interventions left ventricular volume was monitored using a portable radionuclide probe. Isosorbide dinitrate (5 mgm sublingually) while sitting unloads both baroreceptors and the cardiopulmonary receptors; it decreased left ventricular enddiastolic volume (p 〈 0.01) and the mean R—R interval (p 〈 0.005), increased the power of the low-frequency (LF) component of the R—R interval (p 〈 0.01), decreased the power of the high-frequency (HF) component (p 〈 0.005) and increased the LF/HF ratio (p 〈 0.05). The application of cuffs around the thighs in the supine position, which unloads only cardiopulmonary receptors, decreased left ventricular end-diastolic volume (p 〈 0.05) but did not affect mean R—R interval, LF component, HF component and LF/HF ratio (p ⩾ 0.10). Leg raising, which loads only cardiopulmonary receptors, increased left ventricular end-diastolic volume (p 〈 0.05) and did not affect the mean R—R interval, LF component, HF component and LF/HF ratio (p ≥ 0.10). In conclusion, our data suggest that, in normal man, baroreceptor unloading increased sympathetic and decreased parasympathetic neural control of heart rate; cardiopulmonary reflexes do not appear to have a direct neurally mediated effect on heart rate.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01831393
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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