Changes in physical activity among coronary and hypertensive patients: A longitudinal study using the Health Action Process Approach.

OBJECTIVES: Physical activity (PA) is a key factor in cardiovascular disease prevention. Through the Health Action Process Approach (HAPA), the present study investigated the process of change in PA in coronary patients (CPs) and hypertensive patients (HPs). DESIGN: Longitudinal survey study with two follow-up assessments at 6 and 12 months on 188 CPs and 169 HPs. MAIN OUTCOME MEASURES: Intensity and frequency of PA. RESULTS: A multi-sample analysis indicated the equivalence of almost all the HAPA social cognitive patterns for both patient populations. A latent growth curve model showed strong interrelations among intercepts and slopes of PA, planning and maintenance self-efficacy, but change in planning was not associated with change in PA. Moreover, increase in PA was associated with the value of planning and maintenance self-efficacy reached at the last follow-up Conclusions: These findings shed light on mechanisms often neglected by the HAPA literature, suggesting reciprocal relationships between PA and its predictors that could define a plausible virtuous circle within the HAPA volitional phase. Moreover, the HAPA social cognitive patterns are essentially identical for patients who had a coronary event (i.e. CPs) and individuals who are at high risk for a coronary event (i.e. HPs).

Enhanced vascular reactivity in the sympathectomized rat: studies in vivo and in small isolated resistance arteries.

OBJECTIVE: In the conscious rat, sympathectomy (6-hydroxydopamine pretreatment, 100 mg/kg intraperitoneally, twice in the previous 5-6 days) induces, among various homeostatic modifications, the frequent occurrence of sudden and wide oscillations of blood pressure. Since one of the mechanisms underlying this, as yet unexplained, phenomenon may be an enhanced vascular reactivity, we tested the hypothesis that sympathectomized rats exhibit such a hyper-reactivity. We examined the response to a variety of vasoactive agents both in vivo (chronically instrumented conscious animals) and in vitro (small isolated resistance arteries). DESIGN AND METHODS: Wistar-Kyoto sympathectomized rats (6-hydroxydopamine pretreatment, n = 19) and control rats (vehicle pretreatment, n = 23) were studied. In conscious animals, concentration-blood pressure response curves to intra-venous bolus injections of vasopressin, phenylephrine and angiotensin II were obtained. In isolated vessels, concentration-wall tension response curves were obtained for norepinephrine, phenylephrine, vasopressin, serotonin and potassium. Vasodilator responses to acetylcholine (with or without L-NAME), bradykinin and sodium nitroprusside were also evaluated after precontraction with norepinephrine (mesenteric arteries) or vasopressin (cerebral arteries). RESULTS: In sympathectomized rats in vivo the pressor responses to vasopressin, phenylephrine and angiotensin II were significantly larger than in control rats, the difference amounting to 46.5, 40.2 and 57.1%, respectively (all P < 0.05). In vitro, the vascular reactivity of isolated cerebral arteries was similar in sympathectomized and control rats. In contrast, the mesenteric arteries showed significantly increased contractions in sympathectomized compared to control rats in response to norepinephrine, phenylephrine and vasopressin but not to serotonin and potassium, whereas the vasodilator responses to acetylcholine and sodium nitroprusside (but not to bradykinin and acetylcholine+L-NAME) were reduced. CONCLUSIONS: In conclusion, we showed that sympathectomy produces complex alterations of vascular reactivity both in vivo and in isolated vessels, which shift the balance of the sensitivity of the vessel between vasoconstrictor and vasodilating agents towards an increased constriction. These results are unlikely to simply reflect denervation supersensitivity; their underlying receptor, post-receptor and/or contractile mechanisms are yet to be identified.

Sympathovagal interplay in the control of overall blood pressure variability in unanesthetized rats.

The role of sympathetic and parasympathetic influences in the control of overall blood pressure variability was studied in chronically instrumented, freely behaving Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) subjected to sympathectomy by 6-hydroxydopamine (100 micrograms/kg ip) twice in 1 wk (effectiveness verified by abolition of pressor and tachycardic response to tyramine, 150 mg/kg i.v.) and/or to cholinergic blockade by atropine (0.7 mg/kg i.v.). Overall heart rate and blood pressure variabilities were measured as variation coefficients computed beat to beat on 90-min blood pressure recordings. As compared with the vehicle-treated controls, sympathectomized rats had much larger blood pressure variability (WKY, +61%, SHR, +86%, both P < 0.01). Cholinergic blockade superimposed to sympathectomy caused heart rate variability to markedly fall and the already augmented blood pressure variability to further rise 47% in WKY and 28% in SHR (both P < 0.01). Prolonged observation of the animals revealed the systematic occurrence of rapid blood pressure falls occurring at the onset of locomotor activity, accounting for a substantial fraction of the sympathectomy-related increase in blood pressure variability. It is concluded that 1) under undisturbed daily life conditions, sympathetic influences oppose blood pressure variations, presumably by adjusting their vasoconstrictor influences to compensate for the metabolic vasodilation occurring in functionally active tissues; 2) when sympathetic vascular control is lost, vagally mediated heart rate variations oppose the rise in blood pressure variability, possibly via rapid changes in cardiac output that partly offset the fluctuations in total peripheral resistance; and 3) chronic hypertension fails to alter these cardiovascular regulatory mechanisms.

Sympathetic, parasympathetic and non-autonomic contributions to cardiovascular spectral powers in unanesthetized spontaneously hypertensive rats.

OBJECTIVE: To determine whether spectral powers of blood pressure and pulse interval can specifically reflect sympathetic and parasympathetic effects in unanesthetized, free-moving spontaneously hypertensive rats (SHR). DESIGN: Spectral powers were observed before and after various autonomic interventions in chronically instrumented rats. MATERIALS AND METHODS: Chemical sympathectomy was produced in 12-week-old SHR by repeated injections of 6-hydroxydopamine, while control rats were given vehicle alone. Chronic arterial and venous catheters were inserted in the femoral artery and vein. Blood pressure was recorded beat-to-beat for 90 min in free-moving rats; further recording sessions were obtained under additional alpha-receptor blockade with phenoxybenzamine at 1 mg/kg and/or additional cholinergic blockade with atropine at 0.8 mg/kg. Off-line computer analysis (fast Fourier transform) provided estimates of low- (0.025-0.1 Hz), mid- (0.1-0.6 Hz) and high-frequency (0.8-3.0 Hz) powers for blood pressure and pulse interval over consecutive periods of 100 s. RESULTS: The most noticeable findings were that sympathectomy produced a striking increase in the low-frequency power of blood pressure and a tendency (borderline statistical significance) to reduce the mid-frequency power of blood pressure. Additional alpha-receptor blockade had no effect on any spectral power whereas additional cholinergic blockade caused a further increase in the low-frequency blood pressure power and a drastic reduction in all pulse interval powers. CONCLUSIONS: In the unanesthetized SHR, sympathetic activity opposes low-frequency and marginally promotes mid-frequency blood pressure fluctuations; the pulse interval spectral expression of vagal effects is spread throughout the range of frequencies explored and is not confined to the high-frequency band. These data indicate that in SHR no spectral power can specifically reflect the effects of either autonomic limb.

Sympathectomy and cardiovascular spectral components in conscious normotensive rats.

We examined the extent to which sympathetic influences are reflected by spectral powers of blood pressure and pulse interval in specific frequency bands in spontaneously behaving Wistar-Kyoto rats subjected to continuous intraarterial blood pressure recording. The rats were pretreated with 6-hydroxydopamine (150 mg/kg twice in 1 week, n = 19) to produce chemical sympathectomy or received vehicle (n = 15). In the sympathectomized group, additional monitoring sessions were performed with rats under alpha-adrenergic receptor blockade with phenoxybenzamine (n = 8), beta-receptor blockade with propranolol (n = 7), or cholinergic receptor blockade with atropine (n = 8). Blood pressure signals were analyzed by a computer to calculate spectral powers (fast Fourier transform) in the low-frequency (0.025 to 0.1 Hz), mid-frequency (0.1 to 0.6 Hz), and high-frequency (0.8 to 3.0 Hz) bands. In sympathectomized rats, low-frequency power of blood pressure was 70% greater than in intact rats, whereas mid-frequency power was 60% smaller (P < .05 for both) and high-frequency power was unchanged. High-frequency power of pulse interval was also unchanged in sympathectomized rats, whereas low- and mid-frequency powers were reduced by approximately 50% (P < .05). No further alterations in spectral powers were observed by adding alpha- or beta-adrenergic blockade to sympathectomy, whereas adding cholinergic blockade caused a striking reduction in all pulse interval powers. Thus, mid-frequency blood pressure power depends on sympathetic but also to a substantial extent on nonsympathetic influences. Sympathetic influences do not contribute to low-frequency blood pressure power, having instead a restraining effect. The low- and mid-frequency pulse interval powers depend on both sympathetic and vagal influences. Thus, no blood pressure or pulse interval power in the mid- and low-frequency ranges can be regarded as a specific marker of sympathetic activity.

Spontaneous variability of regional haemodynamics in unanaesthetized rats.

AIM: To study the spontaneous variability in regional haemodynamics. METHODS: Twenty normotensive Wistar-Kyoto rats were chronically instrumented with an arterial catheter and with pulsed Doppler flowmeters on the distal aorta, and the superior mesenteric and left renal arteries. After surgical recovery, the rats were monitored in unrestrained conditions. The recorded signals were analysed beat-to-beat to obtain means and coefficients of variation for mean arterial pressure, heart rate, regional blood flow velocity (consecutive 0.8-s periods) and indices of regional vascular resistance (0.8-s ratio of mean arterial pressure to mean blood flow velocity). RESULTS: Muscle and splanchnic blood flow velocities were markedly variable, with coefficients of variation of 12.8 +/- 0.8 and 12.2 +/- 1.7% (means +/- SEM), respectively, about twice as large as the coefficient of variation for mean arterial pressure (6.2 +/- 0.3%). The renal blood flow velocity was slightly less variable than the muscle and splanchnic blood flow velocities, with a coefficient of variation of 10.4 +/- 0.8%, but still markedly and significantly more variable than systemic arterial pressure. A contingency analysis of paired variations in any two given parameters (arterial blood pressure, heart rate, blood flow velocities and indices of vascular resistance) showed a concordant pattern, the only exception being a distinctly discordant trend for the covariations in muscle and splanchnic blood flow velocities. CONCLUSIONS: Regional blood flow velocity and vascular resistance have a larger degree of spontaneous variability than systemic arterial pressure. Renal blood flow velocity is also highly variable, suggesting that short-term stimuli that affect the renal blood vessels are not countered by autoregulation to any great degree. We conclude that while central factors may drive concordant regional haemodynamic variations, some opposing changes in regional blood flow velocity may cancel each other out, thereby reducing the variability in systemic blood pressure.

Cardiac parasympathetic hyperresponsiveness in spontaneously hypertensive rats.

The bradycardic response to baroreceptor stimulation is impaired in human and experimental hypertension. Because this bradycardia mainly depends on the vagus, this may reflect a reduced cardiac parasympathetic responsiveness, which would parallel the reduced cardiac adrenergic responsiveness observed in hypertension. To test this hypothesis, 12-week-old spontaneously hypertensive rats (n = 12) and normotensive Wistar-Kyoto rats (n = 11) were anesthetized with ketamine and underwent bilateral vagotomy. Cardiac parasympathetic responsiveness was assessed from the bradycardia induced by 1) graded electrical stimulation of the right efferent vagus (1-16 Hz) and 2) graded intravenous injections of methacholine (1-8 micrograms.kg-1). The slope of the linear regression between the bradycardiac response and the applied stimulus was taken as the measure of cardiac parasympathetic responsiveness. To identify the onset of possible alterations in cardiac parasympathetic responsiveness in hypertension, the study was extended to younger (8-week-old) spontaneously hypertensive (n = 11) and Wistar-Kyoto (n = 13) rats. With vagal stimulation, cardiac parasympathetic responsiveness was greater in 12-week-old spontaneously hypertensive rats than in 12-week-old Wistar-Kyoto rats (24.8 +/- 5.4 versus 10.1 +/- 1.2 beats per minute per hertz, mean +/- SEM, p less than 0.035). This was also the case with methacholine (18.8 +/- 3.5 versus 13.1 +/- 4.4 beats per minute per microgram per kilogram, p less than 0.045). In contrast, cardiac parasympathetic responsiveness was similar, with both vagal stimulation and methacholine, when tested in the younger spontaneously hypertensive and Wistar-Kyoto groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Potentiation of the baroreceptor-heart rate reflex by sympathectomy in conscious rats.

In both animals and humans, stimuli leading to sympathetic activation are accompanied by an impairment of the baroreceptor-heart rate reflex. To determine whether sympathetic activity normally interferes with this reflex function we examined in conscious Wistar-Kyoto (WKY) rats the effect of chemical sympathectomy by 6-hydroxydopamine on the bradycardic response to baroreceptor stimulation induced by raising blood pressure via intravenous phenylephrine boluses; control rats received vehicle. Spontaneously hypertensive rats were also studied because in these animals there is both a baroreceptor reflex impairment and a sympathetic overactivity. Baroreceptor reflex sensitivity, calculated as the ratio of the peak increase in pulse interval to the peak increase in mean arterial pressure, was 75% greater in sympathectomized WKY rats than in control WKY rats (1.28 +/- 0.15 versus 0.73 +/- 0.10 msec/mm Hg, mean +/- SEM; p less than 0.01). The sympathectomy-induced increase in sensitivity was even larger in spontaneously hypertensive rats (SHR) (1.26 +/- 0.12 versus 0.44 +/- 0.06 msec/mm Hg in sympathectomized SHR versus control SHR, +186%; p less than 0.01) so that the impaired baroreceptor reflex sensitivity observed in control SHR as compared with control WKY rats (-40%, p less than 0.01) was no longer detectable in the sympathectomized groups. To establish whether the sympathectomy-induced potentiation of the reflex was due to an increase in cardiac responsiveness to vagal stimuli, we subjected separate groups of anesthetized, vagotomized SHR and WKY rats to graded electrical stimulation of the right efferent vagus. The bradycardic effects of vagal stimulation, however, were similar in sympathectomized and control animals.(ABSTRACT TRUNCATED AT 250 WORDS)