Cardiovascular autonomic control in mice lacking angiotensin AT1a receptors
| Autor: | Luis F. Joaquim, Helio Cesar Salgado, Yanfang Chen, Rubens Fazan, Mariana Morris, Rogério Brandão Wichi, Vera Farah |
|---|---|
| Přispěvatelé: | Wright State Univ, Universidade Federal de São Paulo (UNIFESP), Universidade de São Paulo (USP) |
| Rok vydání: | 2004 |
| Předmět: |
Angiotensin receptor
medicine.medical_specialty Physiology Ganglionic Blockers Hemodynamics Blood Pressure Baroreflex Autonomic Nervous System Hexamethonium Receptor Angiotensin Type 1 Mice Heart Rate Physiology (medical) Internal medicine Receptors Adrenergic alpha-1 Renin–angiotensin system Heart rate heart rate medicine Animals Telemetry baroreflex Receptor Adrenergic alpha-Antagonists Antihypertensive Agents Mice Knockout business.industry autonomic nervous system blood pressure Prazosin spectral analysis Autonomic nervous system Blood pressure Endocrinology business |
| Zdroj: | Repositório Institucional da UNIFESP Universidade Federal de São Paulo (UNIFESP) instacron:UNIFESP |
| ISSN: | 0363-6119 |
| Popis: | Studies examined the role of angiotensin (ANG) AT1a receptors in cardiovascular autonomic control by measuring arterial pressure (AP) and heart rate (HR) variability and the effect of autonomic blockade in mice lacking AT1a receptors (AT1a-/-). Using radiotelemetry in conscious AT1a-/- and AT1a-/- mice, we determined 1) AP and pulse interval (PI) variability in time and frequency (spectral analysis) domains, 2) AP response to alpha(1)-adrenergic and ganglionic blockade, and 3) intrinsic HR after ganglionic blockade. Pulsatile AP was recorded (5 kHz) for measurement of AP and PI and respective variability. Steady-state AP responses to prazosin (1 mu g/g ip) and hexamethonium (30 mu g/g ip) were also measured. AP was lower in AT1a-/- vs. AT1a-/-, whereas HR was not changed. Prazosin and hexamethonium produced greater decreases in mean AP in AT1a-/- than in AT1a -/-. the blood pressure difference was marked after ganglionic blockade (change in mean AP of -44 +/- 10 vs. -18 +/- 2 mmHg, AT1a-/- vs. AT1a-/- mice). Intrinsic HR was also lower in AT1a-/- mice (431 +/- 32 vs. 524 +/- 22 beats/min, AT1a-/- vs. AT1a-/-). Beat-by-beat series of systolic AP and PI were submitted to autoregressive spectral estimation with variability quantified in low-frequency (LF: 0.1-1 Hz) and high-frequency (HF: 1-5 Hz) ranges. AT1a-/- mice showed a reduction in systolic AP LF variability (4.3 +/- 0.8 vs. 9.8 +/- 1.3 mmHg(2)), with no change in HF (2.7 +/- 0.3 vs. 3.3 +/- 0.6 mmHg2). There was a reduction in PI variability of AT1a-/- in both LF (18.7 +/- 3.7 vs. 32.1 +/- 4.2 ms(2)) and HF (17.7 +/- 1.9 vs. 40.3 +/- 7.3 ms(2)) ranges. the association of lower AP and PI variability in AT1a-/- mice with enhanced AP response to alpha(1)-adrenergic and ganglionic blockade suggests that removal of the ANG AT1a receptor produces autonomic imbalance. This is seen as enhanced sympathetic drive to compensate for the lack of ANG signaling. Wright State Univ, Sch Med, Dept Pharmacol & Toxicol, Dayton, OH 45435 USA Universidade Federal de São Paulo, Sch Med, São Paulo, Brazil Univ São Paulo, Sch Med, BR-14049 Ribeirao Preto, SP, Brazil Universidade Federal de São Paulo, Sch Med, São Paulo, Brazil Web of Science |
| Databáze: | OpenAIRE |
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