Daily exercise and gender influence postexercise cardiac autonomic responses in hypertensive rats.
*Physical Conditioning; Animal; Animals; Atropine Derivatives/pharmacology; Autonomic Nervous System/drug effects/*physiopathology; Exercise Test; Female; Heart Rate/*drug effects; Heart/*innervation; Hypertension/genetics/*physiopathology; Inbred SHR; Male; Metoprolol/pharmacology; Nitroglycerin/pharmacology; Phenylephrine/pharmacology; Rats; Running; Sex Characteristics; Sympathetic Nervous System/drug effects/*physiopathology; Weight Loss
The influence of daily spontaneous running (DSR) and gender on postexercise cardiac autonomic responses was examined in spontaneously hypertensive rats. Rats were weaned at 4-5 wk of age and were randomly assigned to a sedentary (7 males and 6 females) or DSR (7 males and 8 females) group. After 8 weeks of DSR or sedentary control, rats were chronically instrumented with arterial and venous catheters. After 5 days of recovery, cardiac sympathetic (ST) and parasympathetic tonus (PT) were determined (by the response of heart rate to receptor antagonists) on alternate days under two experimental conditions: no exercise and postexercise. After a single bout of dynamic treadmill exercise (12 m/min, 10% grade for 40 min) ST was reduced (P \textless 0.05) (male sedentary: no exercise 45 +/- 4 vs. postexercise 28 +/- 3 beats/min; female sedentary: no exercise 69 +/- 10 vs. postexercise 37 +/- 7 beats/ min). PT was also altered after exercise (male sedentary: no exercise -31 +/- 4 vs. postexercise -11 +/- 2 beats/min; female sedentary: no exercise -5 +/- 4 vs. postexercise 7 +/- 4 beats/min). After DSR, ST was reduced (male sedentary 45 +/- 4 vs. DSR 22 +/- 3 beats/min; female sedentary 69 +/- 10 vs. DSR 36 +/- 4 beats/min) (P \textless 0.05). Finally, male rats had a lower ST and higher PT than female rats. These results demonstrate that 1) ST was reduced after a single bout of dynamic exercise; 2) ST was reduced after DSR; 3) the autonomic response to acute exercise was attenuated after DSR; and 4) there was a gender influence on the cardiac autonomic function.
Chen Y; Chandler M P; DiCarlo S E
The American journal of physiology
1997
1997-03
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajpheart.1997.272.3.H1412" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1997.272.3.H1412</a>
Myocardial work load is a major determinant of norepinephrine-induced left ventricular dysfunction.
Anesthesia; Animals; Blood Pressure/*drug effects; Cardiovascular; Consciousness; Diastole/drug effects; Dose-Response Relationship; Drug; General; Heart Rate/*drug effects; Heart/drug effects/*physiology; Left/drug effects/*physiology; Models; Norepinephrine/*pharmacology; Pentobarbital; Rabbits; Systole/drug effects; Time Factors; Ventricular Function
This study was conducted to determine whether increased myocardial energy demand plays a role in norepinephrine (NE)-induced left ventricular (LV) dysfunction. A range of arterial pressure-heart rate (P-R) products (myocardial energy demand) was produced in both conscious and pentobarbital sodium-anesthetized rabbits with the same dose of NE (10 micrograms priming bolus plus 2.5 micrograms.kg-1 x min-1 for 2.5 h). After NE treatment, LV function was evaluated in vitro and found to be markedly diminished in the rabbits that had an elevated P-R product. In contrast, LV function was not significantly affected when the P-R product was maintained near control levels during NE treatment. In separate experiments, rabbit hearts were isolated and exposed to NE (10,000 or 50,000 pg/ml) for 2.5 h under low P-R product conditions. These hearts exhibited a dose-dependent decrease in LV function that was modest compared with that observed in rabbits that had elevated P-R products during in vivo NE treatment. Our results suggest that high concentrations of NE may cause modest degrees of LV dysfunction independently of increases in myocardial energy demand, but the LV dysfunction is exacerbated when myocardial energy demand is elevated.
Bosso F J; Allman F D; Pilati C F
The American journal of physiology
1994
1994-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajpheart.1994.266.2.H531" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1994.266.2.H531</a>