Post-exercise elevations in sympathetic nerve activity and baroreflex function in normotensive rabbits.

We tested the hypothesis that a single bout of dynamic exercise reduces post-exercise arterial pressure, heart rate, and renal sympathetic nerve activity and attenuates the arterial baroreflex control of heart rate and renal sympathetic nerve activity in normotensive New Zealand White rabbits. Animals were chronically instrumented with right jugular venous and left femoral arterial catheters, and electrodes around the renal sympathetic nerve. Arterial pressure, heart rate, and renal sympathetic nerve activity were recorded for two hours pre-exercise and two hours after a single bout of treadmill exercise (post-exercise). Post-exercise heart rate, arterial pressure, and renal sympathetic nerve activity were elevated above pre-exercise values (71+/-3 bpm, 13+/-1 mmHg, and 80+/-21%, respectively). These data demonstrate that normotensive rabbits do not exhibit post-exercise hypotension, due in part to elevations in sympathetic nerve activity. In addition, arterial baroreflex regulation of heart rate and renal sympathetic nerve activity were determined pre- and post-exercise. Exercise shifted the baroreflex function curve for heart rate and renal sympathetic nerve activity upward and to the right without a change in gain. These data suggest that post-exercise elevations in sympathetic nerve activity are due, in part, to an elevation of the operating point of the arterial baroreflex to a higher pressure. These responses in normotensive rabbits contrast sharply with the responses in hypertensive individuals and animals. Understanding the mechanisms contributing to the differences between hypertensive and normotensive subjects may lead to measures designed to lower arterial pressure in hypertensive individuals.

Reduced vascular responsiveness after a single bout of dynamic exercise in the conscious rabbit.

We measured agonist-induced changes in the iliac artery blood flow velocity (IFV) independent of baroreflex-mediated compensatory mechanisms in chronically instrumented New Zealand White rabbits (n = 8). Animals were instrumented with a Doppler flow probe around the right common iliac artery. A Teflon catheter was inserted into the right iliolumbar artery for local infusion of the vasoactive agonists. Another Teflon catheter was inserted in the left femoral artery for the measurement of pulsatile and mean arterial (MAP) blood pressures and heart rate (HR). The alpha-adrenergic receptor agonist phenylephrine (PE, 1.32-10.0 micrograms), the beta 1- and beta 2-adrenergic receptor agonist isoproterenol (IP, 0.022-0.11 micrograms), and the purinergic receptor agonist adenosine (AD, 10.0-100.0 micrograms) were injected into the functionally isolated hindlimb, and dose-response curves were generated. Changes in IFV were obtained without changes in MAP or HR. Exercise increased HR, MAP, and IFV (65.3 +/- 7.1 beats/min, 11.1 +/- 2.2 mmHg, and 2.2 +/- 0.3 kHz, respectively). The maximum responses to PE, AD, and IP were reduced 29.0 +/- 6.7, 50.7 +/- 8.5, and 61.0 +/- 8.1%, respectively, after exercise. In conclusion, exercise attenuated adrenergic and purinergic receptor-mediated vascular responses in the intact conscious rabbit.

Acute exercise attenuates phenylephrine-induced contraction of rabbit isolated aortic rings.

Factors associated with a single bout of dynamic exercise (increased circulating catecholamines, increased body temperature, and decreased pH) are known to attenuate the vascular response to alpha-adrenergic receptor activation. Therefore, we postulate that an acute bout of dynamic exercise may decrease the vascular response to catecholamines. To test this hypothesis, we evaluated contractile responsiveness to phenylephrine (PE) in aortae of two groups of New Zealand white rabbits, a control group (no exercise) and an exercise group (treadmill running, 24m.min-1; 16 +/- 2.0 min). Aortic rings were prepared from age-matched control (N = 6) and exercise rabbits (N = 5) and mounted for isometric tension recording (in Krebs-Henseleit-bicarbonate solution, 37 degrees C, 1.5 g passive tension). After equilibration (2 h) a cumulative concentration-response curve to PE (10(-7) M-10(-2) M) was obtained. The results demonstrate that a single bout of dynamic exercise attenuates (P < 0.05) the maximal contractile tension (2,457 +/- 120 vs 3,620 +/- 321 mg tension.mg-1 ring wt), gain (602 +/- 31 vs 878 +/- 87 mg.M-1 PE), and rate of contraction (6.2 +/- 0.3 vs 4.7 +/- 0.3 mg tension.s-1). In addition, contraction threshold was significantly increased in exercise (2.6 +/- 0.4 x 10(-6) M) vs control aortae (1.03 +/- 0.4 x 10(-6) M). A single bout of dynamic exercise did not alter the contractile response to 70 mM KCl (3,555 +/- 270 vs 3,083 +/- 233 mg tension.mg-1 ring weight). These data suggest that an acute bout of dynamic exercise significantly attenuates alpha-adrenergic receptor-mediated contraction of vascular smooth muscle.

Regulation of transcription of the Bacillus subtilis spoIIA locus.

The start point of spoIIA transcription was defined by primer extension analysis with two separate primers. It was 27 bases upstream from the putative translation initiation codon of the first open reading frame in the spoIIA locus. A region extending at least 52 bases upstream from the transcription start site was necessary for transcription, as determined with integrative plasmids. Transcription of spoIIA was dependent on the spoOA, spoOB, and spoOF loci, but this dependency was partly overcome by increasing the number of copies of the spoIIA promoter region. Transcription of spoIIA was absolutely dependent on the spoOH locus, which codes for the RNA polymerase sigma factor sigma H. Regions approximately -35 and -10 upstream from the spoIIA transcription start site showed sequence homology with Bacillus subtilis sigma H promoters.