Interaction between cholinergic and nitrergic vasodilation: a novel mechanism of blood pressure control
| Autor: | Urs Scherrer, Mattia Lepori, Hervé Duplain, Pascal Nicod, Claudio Sartori |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2017 |
| Předmět: |
Adult
Atropine Male medicine.medical_specialty Adrenergic beta-Antagonists/pharmacology Adult Arginine/*pharmacology Atropine/*pharmacology Cardiac Output/drug effects Enzyme Inhibitors/pharmacology Female Hemodynamic Processes/drug effects Humans Leg Male Muscarinic Antagonists/*pharmacology Nitric Oxide Synthase/*antagonists & inhibitors Phenylephrine/pharmacology Propranolol/pharmacology Regional Blood Flow/drug effects Statistics Nonparametric Vasoconstrictor Agents/*pharmacology omega-N-Methylarginine/*pharmacology Physiology Adrenergic beta-Antagonists Vasodilation Muscarinic Antagonists 030204 cardiovascular system & hematology Arginine Sudden death Statistics Nonparametric Nitric oxide Phenylephrine 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Physiology (medical) Internal medicine Humans Vasoconstrictor Agents Medicine Cardiac Output Enzyme Inhibitors 030304 developmental biology Leg 0303 health sciences omega-N-Methylarginine biology business.industry Hemodynamics Propranolol 3. Good health Nitric oxide synthase Endocrinology Blood pressure medicine.anatomical_structure chemistry Regional Blood Flow biology.protein Vascular resistance Cholinergic Female Nitric Oxide Synthase medicine.symptom Cardiology and Cardiovascular Medicine business Vasoconstriction |
| Zdroj: | Cardiovascular Research, vol. 51, no. 4, pp. 767-72 |
| Popis: | OBJECTIVE: Cholinergic vasodilation has been thought to play little if any role in the regulation of blood pressure in humans. Autonomic denervation potentiates the vasoconstriction evoked by nitric oxide synthase inhibition in humans, but the mechanism is unclear. We hypothesized that this may be related to loss of neuronal, non-nitric-oxide-dependent vasodilation. METHODS: To test this hypothesis, we examined effects of cholinergic blockade on blood pressure, heart rate and peripheral vascular responses to systemic infusion of the nitric-oxide-dependent vasoconstrictor L-NMMA (0.5 mg/kg/min over 15 min) in eight normal subjects. RESULTS: The L-NMMA-induced increase in mean (+/-S.E.) arterial pressure was roughly three times larger (P=0.002) in the presence than in the absence of cholinergic blockade (38+/-6 vs. 13+/-2 mmHg). Similarly, the increase in systemic and calf vascular resistance was more than twofold larger during L-NMMA-atropine. This potentiation was specific for nitric-oxide-dependent vasoconstriction, because atropine did not alter the responses to phenylephrine infusion. Cholinergic blockade also altered (P=0.004) the heart rate response to nitric oxide synthase inhibition; during L-NMMA alone heart rate decreased by 10+/-2 beats/min, whereas during L-NMMA-atropine infusion it increased by 14+/-4 beats/min. CONCLUSION: Cholinergic mechanisms play an important hitherto unrecognized role in offsetting the hypertension and cardiac sympathetic activation caused by nitric oxide synthase inhibition in humans. Decreased parasympathetic activity and impaired nitric oxide synthesis characterize several cardiovascular disease states, as well as normal aging. The conjunction of these two defects could trigger sudden death and contribute to the hypertension of the elderly. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|