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At least 1,117 records · Page 62Linked to original sources
PubMed1985

Hypotensive actions of ketanserin in dogs: involvement of a centrally mediated inhibition of sympathetic vascular tone.

The intravenous (i.v.) administration of ketanserin (0.1-0.4 mg/kg) produced immediate and sustained decreases in systemic blood pressure and heart rate in pentobarbitone-anaesthetized dogs. These doses of ketanserin did not inhibit common carotid vasoconstrictor responses to intraarterial (i.a.) noradrenaline, pre-ganglionic stimulation of the sectioned cervical sympathetic nerve, or i.v. nicotine, thus the effects of ketanserin are not due to blockade of vascular alpha-adrenoceptors, adrenergic neurone blockade, or ganglionic blockade. Systemic pressor responses to i.v. nicotine, which produces sympathetic activation by both central and ganglionic stimulating actions, and to common carotid artery occlusion, were inhibited by 0.1-0.4 mg/kg of ketanserin i.v. These results suggest that in the anaesthetized dog, the hypotensive action of ketanserin involves a centrally mediated inhibition of sympathetic tone. Peripheral vascular 5-HT2 receptor blockade does not appear to be responsible for the hypotensive effect of ketanserin in this model, although this does not preclude the involvement of such a mechanism in its clinical antihypertensive action.

Animals↗
PubMedDate not supplied

Regulation of coronary blood flow.

A very schematic summary of possible factors that affect coronary vascular resistance is illustrated in Fig. 11. These factors are mechanical, myogenic, metabolic, and neural. Mechanical influence is passive and is essentially determined by the extravascular compression which is important only during systole and particularly in the subendocardial layers of the left ventricular myocardium. With respect to the myogenic factor it is controversial whether it plays a role in adjustments of coronary vascular tone. Metabolic processes are possibly integrated at the level of the myocardial cell PO2 which is the resultant of oxygen supply and need, which in turn depend on the myocardial contractile activity as well as other biochemical processes. A decrease in myocardial PO2 gives rise to the release of the vasodilator metabolite adenosine. Nevertheless, other chemical factors (H+, K+, osmolarity) known to be released by the heart (which by themselves are poor and transient coronary vasodilators and whose release does not correspond with changes in coronary resistance) may play a role by modulating the coronary sensitivity to adenosine and other factors.

Adenosine↗
PubMedDate not supplied

Suprabulbar and bulbar integration of ventilation and ear vascular control during thermoregulation in the rabbit.

Suprabulbar and bulbospinal integration of cardiorespiratory responses to cold and heat stress was studied in groups of normal, thalamic and pontine rabbits. The animals sat in an airconditioned environmental chamber in which ambient temperature (TA) was maintained sequentially at 22 degrees C, 12 degrees C, 22 degrees C and 35 degrees C, with an accuracy of +/- 1 degree C. Neither thalamic nor pontine rabbits could maintain core temperature in cold or heat. At TA 35 degrees C, thalamic and pontine animals did not pant, indicating that telencephalic responses were necessary for the integration of mechanisms promoting respiratory heat loss. Thalamic animals, however, could inhibit ear vascular sympathetic tone in the heat, but the response was absent in pontine animals, suggesting diencephalic responses were essential for the integration of mechanisms promoting ear skin heat loss. Thus, the neural adjustments to thermal stress depend on mechanisms of integration distributed longitudinally throughout the central nervous system, and different components of the reflex cardiorespiratory response depend on different sites in the central nervous system for their full expression.

Animals↗
PubMed1984

Guanethidine-sensitive release of neuropeptide Y-like immunoreactivity in the cat spleen by sympathetic nerve stimulation.

Splenic nerve stimulation (10 Hz for 2 min) caused a perfusion-pressure increase, a volume reduction and an increase in the output of neuropeptide Y-like immunoreactivity (NPY-LI) from the isolated blood-perfused cat spleen. Gel-filtration HPLC analysis revealed that plasma NPY-LI collected during nerve stimulation was similar to the NPY-LI in the spleen and synthetic porcine NPY. Combined propranolol and phenoxybenzamine pretreatment enhanced NPY output upon nerve stimulation by about 60%. Forty percent of the perfusion-pressure increase and 25% of the volume reduction seen during control stimulations remained after adrenoceptor blockade. Guanethidine abolished the release of NPY-LI, the perfusion-pressure increase and the volume reduction normally seen upon splenic nerve stimulation. Infusion of synthetic porcine NPY caused a long-lasting increase in perfusion pressure and a relatively moderate volume reduction. Noradrenaline (NA) both increased perfusion pressure and induced a marked volume reduction. The NPY effects were resistant to adrenoceptor antagonists in doses which abolished the NA response. In conclusion, the present data show that NPY-LI is released upon sympathetic nerve stimulation by a guanethidine-sensitive mechanism. Furthermore, the sympathetic response is partially resistant to adrenoceptor antagonists and NPY has powerful vasoconstrictor effects. This provides further evidence for a role of NPY in sympathetic vascular control.

Animals↗
PubMed2004

Human autonomic responses to blood donation.

In order to characterize autonomic responses to acute volume loss, supine ECG, blood pressure (BP) and uncalibrated breathing signal (UBS) recordings were taken before and after blood donation in 48 healthy volunteers. Time and frequency domain parameters of RR interval (RRI), BP and UBS variability were determined. Baroreflex gain was calculated by the technique of the spontaneous sequences and cross-spectral analysis. The systolic (SAP), diastolic (DAP) and mean BP (MAP) increased after the blood withdrawal. The central frequency of breathing and mean heart rate did not change. RRI variability increased in low frequency band (LF), tended to decrease in high frequency band (HF). Systolic BP variability increased in both frequency bands, but was statistically significant only in the high frequency band. Diastolic BP power increased in both frequencies. From the different baroreflex gain estimates, up sequence BRS and HF alpha index decreased significantly. The phase angle between RRI and systolic blood pressure powers in LF band did not change (-58 +/- 24 degrees and -54 +/- 26 degrees ). In the high frequency range, the phase became more negative (-1 +/- 29 degrees and -17 +/- 32 degrees, p = 0.001). The withdrawal of 350-400 ml blood in 5 min resulted in sympathetic activation, which was reflected in increased systolic, diastolic and mean BP. The increased BP oscillation was a sensitive marker of the minor volume depletion. This was coupled by increased RRI oscillation via baroreflex mechanisms in the LF band. Changes in the RRI and BP oscillations in the HF band showed no similar coupling. That points to the fact that RRI oscillations in this band should not be explained entirely by baroreflex mechanisms. Vagal withdrawal was reflected in decreased root mean square of successive differences (RMSSD), decreased HF RRI power and decreased up sequence BRS.

Adolescent↗
PubMed2000

Role of angiotensin II in regulation of basal and sympathetically stimulated vascular tone in early and advanced cirrhosis.

BACKGROUND & AIMS: The renin-angiotensin and sympathetic nervous systems are activated in cirrhosis. This study aimed to establish the role of angiotensin II (ANG II) in the regulation of basal and sympathetically stimulated vascular tone in preascitic cirrhotic patients and patients with diuretic-refractory ascites compared with age- and sex-matched healthy controls. METHODS: Forearm blood flow (FBF) responses to lower body negative pressure (LBNP) and to subsystemic, intrabrachial infusions of losartan, an angiotensin II type 1 (AT(1)) receptor antagonist, norepinephrine, and ANG II were measured using venous occlusion plethysmography. RESULTS: In all groups, ANG II and norepinephrine caused dose-dependent reductions in FBF (P < 0.001); responses to norepinephrine were similar across the 3 groups but those to ANG II were less in both cirrhotic groups than in controls (P < 0.01). Losartan caused a dose-dependent increase in FBF only in patients with refractory ascites (P < 0.01). LBNP caused less reduction in FBF in refractory ascites patients than in both preascitic patients and controls (P < 0.01). CONCLUSIONS: Despite hyporesponsiveness to exogenous ANG II in both early and advanced cirrhosis, endogenous ANG II contributes to the maintenance of basal vascular tone only in advanced cirrhosis. These findings suggest a role of ANG II in the pathogenesis of ascites. Attenuated LBNP responses occurred only in advanced cirrhosis, without apparent interaction with endogenous ANG II.

Adult↗
PubMed2003

Examination of normalized pulse volume-blood volume relationship: toward a more valid estimation of the finger sympathetic tone.

The pulsatile ac component (DeltaI) superimposed on the transmitted dc components (I: tissue plus blood) are obtained from a near-infrared finger photoplethysmogram using a wavelength of 810 nm. Only the dc component is given in an ischaemic circulatory state (I(t): tissue only). Based on Lambert-Beer's law, normalized pulse volume (NPV; =DeltaI/I) and blood volume [BV; =ln(I(t)/I)] have recently been advocated as quantitative measures. In this study, the NPV-BV relationship was examined using the finger occlusion method during rest and mental arithmetic in 16 female undergraduates. Finger vascular tone during stress was evaluated by the distance of the linear and parallel NPV-BV regression lines (D(NB)) between rest and stress conditions. A reference standard was provided by the linear regression lines of compliance index (CI=NPV/pulse pressure) and BV to the transmural pressure. The estimates at 40 mmHg of transmural pressure, as an arbitrarily chosen reference point, were calculated (CI40 and BV40). D(NB) correlated well with them (r=0.81 and 0.94, respectively). The multiple regression with mean blood pressure indicated that the combination of D(NB) and the reactivities in heart period could explain approximately 50% of valiance in pressor response. In conclusion, D(NB) is easily obtainable from the NPV-BV function and seems to be more specific and valid than NPV as an index of finger sympathetic tone, since it adjusts the mechanical effect of arterial distending pressure.

Adult↗
PubMed2002

Is lead exposure the principal cause of essential hypertension?

Lead is a ubiquitous toxin, known to have adverse effects on the body even at low levels of exposure. In this review we explore whether low lead may be the principal or a major contributory cause of essential hypertension, and whether removal of lead from the environment may eventually reduce both the overall incidence of hypertension and the increased incidence with aging.

Animals↗