Effect of Baroreceptor Deafferentation on Central Catecholamines in the Rat

1979 ◽  
Vol 57 (s5) ◽  
pp. 221s-223s ◽  
Author(s):  
Margaret A. Petty ◽  
J. P. Chalmers ◽  
M. Brown ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Tyrosine Hydroxylase ◽  
Brain Stem ◽  
Hydroxylase Activity ◽  
Methyltransferase Activity ◽  
Neurogenic Hypertension ◽  
Noradrenaline Synthesis ◽  
Noradrenaline And Adrenaline ◽  
Sympathetic Efferent Activity

1. Sinoaortic deafferentation in the rat leads to increased blood pressure and heart rate. 2. Early increases in tyrosine hydroxylase activity both in brain stem and hypothalamus suggest that increased noradrenaline synthesis may contribute to the development of neurogenic hypertension. 3. After 4 weeks, phenylethanolamine-N-methyltransferase activity was reduced in the hypothalamus. 4. Noradrenaline- and adrenaline, but not dopamine-containing neurones may participate in regulation of sympathetic efferent activity.

Effects of Prizidilol (SKF 92657) on Blood Pressure, Haemodynamics, Sympathetic Nervous System Activity and Plasma Volume in Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 465s-468s ◽  
Author(s):  
R. Fariello ◽  
C. L. Alicandri ◽  
E. Agabiti-Rosei ◽  
G. Romanelli ◽  
M. Castellano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Volume ◽  
Antihypertensive Effect ◽  
Blood Pressure Reduction ◽  
Cardiac Performance ◽  
Plasma Aldosterone ◽  
Nervous System Activity ◽  
Peripheral Vasodilatation ◽  
Noradrenaline And Adrenaline

1. The antihypertensive effect of 4 weeks' treatment with prizidilol (SKF 92657) (mean dosage 520 mg once or twice daily) was studied in ten essential hypertensive patients. 2. Both systolic and diastolic blood pressure were significantly reduced in all cases. Supine heart rate did not change, and in the erect position heart rate was significantly lowered. 3. Blood pressure reduction was due to peripheral vasodilatation, as the cardiac index increased after 4 weeks of prizidilol treatment. 4. After prizidilol plasma noradrenaline and adrenaline increased significantly, and PRA and plasma aldosterone were reduced. Although plasma volume increased, body weight did not change. 5. Cardiac performance, as evaluated by the PEP/LVET ratio, improved after treatment with prizidilol.

Effects of opioid antagonism on the haemodynamic and hormonal responses to exercise

1988 ◽  
Vol 75 (3) ◽  
pp. 293-300 ◽  
Author(s):  
Jan Staessen ◽  
Roberto Fiocchi ◽  
Roger Bouillon ◽  
Robert Fagard ◽  
Peter Hespel ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Serum Insulin ◽  
Plasma Renin ◽  
Endogenous Opioids ◽  
Renin Activity ◽  
Plasma Adrenaline ◽  
Noradrenaline And Adrenaline

1. Physical effort involves, along with an increase in the plasma concentration of β-endorphin, profound adaptations of the circulation and the endocrine system. The effects of opioid antagonism on the responses of blood pressure, heart rate and several hormones to exercise were therefore studied in 10 normal men. They exercised in the supine position up to 33% and 66% of their maximal exercise capacity and received in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg intravenously, followed by a continuous infusion of 10 mg/h). 2. Intra-arterial pressure and heart rate were continuously monitored, but were not affected by naloxone. 3. At rest, opioid antagonism produced a rise in plasma renin activity and in plasma adrenocorticotropin, Cortisol and aldosterone, but only the stimulation of the two adrenocortical hormones differed significantly from the control experiments; at rest naloxone also prevented the fall in plasma adrenaline, which occurred with saline infusion. Furthermore, the exercise-induced rises in plasma angiotensin II, aldosterone, Cortisol, noradrenaline and adrenaline were higher on naloxone than on saline, while a similar tendency was also present for the increases with exercise in plasma renin activity and plasma adrenocorticotropin. Neither at rest nor during exercise did opioid antagonism alter plasma lactate and glucose and serum insulin and growth hormone. 4. In conclusion, (1) endogenous opioids are not involved in the responses of blood pressure and heart rate to supine exercise; (2) at rest and during exercise, the endogenous opioids inhibit the secretion of adrenocorticotropin, aldosterone, Cortisol, noradrenaline and adrenaline; (3) they also inhibit the plasma renin-angiotensin II system indirectly via the catecholamines.

Localization of Central Noradrenergic Mechanisms in Cardiovascular Regulation in Rats

1974 ◽  
Vol 48 (s2) ◽  
pp. 277s-278s ◽  
Author(s):  
H. Struyker Boudier ◽  
G. Smeets ◽  
G. Brouwer ◽  
J. Van Rossum
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Brain Stem ◽  
Cardiovascular Regulation ◽  
Anterior Hypothalamus ◽  
Anaesthetized Rats ◽  
Lower Brain Stem ◽  
The Brain

1. Various drugs were injected stereotactically into the brain of anaesthetized rats. 2. Noradrenaline injected into the area of the nucleus of the tractus solitarius in the lower brain stem or into the far anterior hypothalamus/pre-optic region induced a fall in blood pressure and in heart rate related to the administered dose. 3. When injected into the anterior hypothalamus/pre-optic region, clonidine and alpha-methyl-noradrenaline induced a long-lasting decrease in blood pressure and heart rate.

scholarly journals The Effects of Gallamine and a Mixture of Pancuronium and Alcuronium on the Pressor and Plasma Catecholamine Responses to Tracheal Intubation

1984 ◽  
Vol 12 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Mary F. Cummings ◽  
W. J. Russell ◽  
D. B. Frewin ◽  
Wendy A. Miller
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Tracheal Intubation ◽  
Arterial Pressure ◽  
Plasma Noradrenaline ◽  
Plasma Catecholamine ◽  
Plasma Adrenaline ◽  
Noradrenaline Concentration ◽  
Noradrenaline And Adrenaline

Tracheal intubation can be accompanied by significant increases in arterial pressure, heart rate and the plasma levels of noradrenaline and adrenaline. The drugs used at induction can enhance or attenuate these responses. In nine patients who had received gallamine, intubation was associated with a 45% rise in mean arterial pressure, a twofold rise in plasma adrenaline and a 49% rise in plasma noradrenaline concentration. When a mixture of pancuronium and alcuronium (in a ratio of 4:10 by weight) was used in ten patients, blood pressure fell 24% after induction and rose 49% after intubation. A 24% rise in plasma noradrenaline in response to intubation was also observed. Compared with pancuronium alone, the use of the mixture attentuates the rise in blood pressure and noradrenaline concentration associated with intubation but does not abolish them. In addition, the mixture was associated with a significant fall in blood pressure between induction and intubation, whereas this was not found with gallamine.

Cardiovascular actions of microinjections of angiotensin II in the brain stem of rats

1984 ◽  
Vol 246 (5) ◽  
pp. R811-R816 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Brain Stem ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Ang Ii ◽  
The Brain

The blood pressure and heart rate responses to microinjection of angiotensin II (ANG II) into the brain stem of urethan-anesthetized rats were studied. Microinjection of ANG II into the area postrema (AP) resulted in significant elevation of blood pressure and significant reduction of heart rate. Microinjection into the region of the nucleus tractus solitarius (NTS) yielded a significant dose-dependent elevation in blood pressure and consistent increases in heart rate. The response to microinjection of ANG II into the region of the NTS was not due to leakage into the peripheral circulation, since intravenous administration of the ANG II antagonist, saralasin, did not attenuate the response. In fact, the cardiovascular response was increased after peripheral ANG II blockade, and the heart rate, which was consistently but not significantly elevated by NTS injection alone, was significantly elevated after saralasin pretreatment. Thermal ablation of the AP did not change the heart rate or the pressor response to microinjection of ANG II into the region of the NTS, indicating that the response was not mediated through the AP.

Fastigial nucleus cardiovascular response and brain stem lesions in the beagle

1986 ◽  
Vol 250 (2) ◽  
pp. H231-H239 ◽  
Author(s):  
K. J. Dormer ◽  
J. A. Andrezik ◽  
R. J. Person ◽  
J. T. Braggio ◽  
R. D. Foreman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Electrical Stimulation ◽  
Brain Stem ◽  
Kainic Acid ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Fastigial Nucleus ◽  
Reticular Nucleus ◽  
A5 Area

Changes in the excitatory cardiovascular response (heart rate, arterial blood pressure, left ventricular pressure, and LV dP/dt as an index of myocardial contractility) resulting from electrical stimulation of the cerebellar fastigial nucleus (FN) were recorded after placement of DC or radio-frequency lesions or after microinjections of kainic acid into brain stem areas that receive FN projections and have been shown to be involved in central cardiovascular control. FN-induced increases in heart rate, blood pressure, and contractility were reduced or abolished by lesions made in the restiform body or the A5 area, which is homologous to the catecholamine-containing region in cats and rats. Lesions in the paramedian reticular nucleus, rostral and caudal to obex, failed to reduce the FN cardiovascular response. Nucleus of the solitary tract lesions augmented the FN pressor response and tachycardia. Kainic acid (1 microliter of 100 mM solution) caused profound depression of heart rate, blood pressure, and contractility and reduced or eliminated the FN-induced cardiovascular response when injected into the A5 area, previously identified by the pressor response following electrical stimulation. We concluded from these observations that a descending fastigiobulbar sympathoexcitatory pathway courses through a previously identified A5 pressor area that is also capable of a depressor response when the cell bodies alone are activated.

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