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[Changes in humoral pressor and depressor factors in essential hypertension during lisinopril therapy]
J Peleska1, K Horký, M Jáchymová
1II. interní klinika a Kardiologická laborator, 1. LF UK, Praha.
Insights
Essential hypertension involves metabolic and cellular changes. Angiotensin converting enzyme inhibitors like lisinopril show promise, impacting urinary kallikrein, plasma adrenalin, and blood viscosity in hypertensive patients.
Area of Science:
- Cardiology and Hypertension Research
- Endocrinology and Metabolic Disorders
- Pharmacology and Therapeutics
Context:
- Arterial hypertension is a complex multifactorial disease, not just a blood pressure regulation issue.
- Metabolic and cellular deviations are integral to understanding hypertension.
- Angiotensin converting enzyme (ACE) inhibitors are a promising therapeutic class.
Purpose:
- To investigate the effects of lisinopril on pressor and depressor humoral indicators in hypertensive patients.
- To compare these indicators in patients with essential hypertension (Stage I and II) before and after treatment with ACE inhibitor lisinopril.
- To compare findings with normotensive healthy subjects.
Summary:
- Hypertensive patients exhibited lower urinary kallikrein, higher basal and glucose-load plasma adrenalin, and increased relative plasma viscosity compared to normotensives.
- No significant differences were observed in plasma renin activity, plasma aldosterone, fibrinogen, or urinary prostaglandins between groups.
- A glucose load elevated plasma renin, aldosterone, and noradrenaline in both normotensive and hypertensive individuals, irrespective of lisinopril treatment.
Impact:
- This study provides insights into the multifactorial nature of hypertension and the comprehensive effects of ACE inhibitors.
- Findings may inform therapeutic strategies by highlighting specific biomarkers affected by hypertension and its treatment.
- Understanding these humoral and cellular deviations is crucial for developing more effective hypertension management.
Abstract:
Arterial hypertension is nowadays no longer considered an isolated disorder of blood pressure regulation but a multifactorial disease with metabolic and cellular deviations. From the therapeutic aspect of thus conceived hypertension today inhibitors of the angiotensin converting enzyme seem most promising. With regard to their assumed comprehensive effect, the authors investigated simultaneously selected pressor and depressor humoral indicators and other indicators in 21 hypertensive patients with stage I and II of essential hypertension before and after three-month treatment with an angiotensin converting enzyme inhibitor lisinopril (Prinivil, Merck, Sharp and Dohme) and compared them with findings in 21 normotensive healthy subjects. Hypertensive subjects before treatment had, as compared with normotensives, significantly lower urinary kallikrein (7.8 +/- 1.2 < 18.0 +/- 4.2 EU/24hr, a significantly higher basal plasma adrenalin (1.27 +/- 0.20 > 0.54 +/- 0.20 pmol/ml) and adrenalin after a glucose load (1.26 +/- 0.22 > 0.51 +/- 0.12) and a higher relative plasma viscosity (1.74 +/- 0.02 > 1.67 +/- 0.01). The two groups did not differ significantly as to the plasma renin activity, plasma aldosterone and fibrinogen concentration and the level of urinary prostaglandins per 24 hr: 6-keto-prostaglandin F1a, thromboxane B2 and prostaglandins E and F2a. The 75 g glucose load produced an increased plasma renin, aldosterone and noradrenaline activity in normotensives as well as hypertensives before and after lisinopril treatment.(ABSTRACT TRUNCATED AT 250 WORDS)