Influence of the sympathetic nervous system and vasopressin on the blood pressure lowering effect of nifedipine in deoxycorticosterone acetate–salt hypertensive rats

1987 ◽  
Vol 73 (3) ◽  
pp. 253-258 ◽  
Author(s):  
Yutaka Takata ◽  
Yoshiaki Yamashita ◽  
Shuichi Takishita ◽  
Masatoshi Fujishima
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Calcium Influx ◽  
Hypotensive Effect ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Blood Pressure Lowering Effect ◽  
Hypotensive Action ◽  
Sympathetic Nervous

1. The role of the sympathetic nervous system and the effect of vasopressin (AVP) on the hypotensive action of nifedipine (Nf) were evaluated in conscious, unrestrained normotensive and DOCA–salt hypertensive rats. 2. The hypotensive response to Nf was much greater in DOCA rats than in the controls. 3. Solitary blockade of the sympathetic nervous system or AVP, did not alter the Nf effect in either DOCA or control rats. However, a combination clearly diminished the effect of Nf in the DOCA group, but enhanced it in the controls. The inhibition of angiotensin II (ANG II) augmented the hypotensive effect of Nf in control animals, but not in the DOCA rats. The percentage fall in blood pressure with Nf was much the same in both groups after the combined inhibition of the sympathetic nervous system and AVP. 4. The enhanced hypotensive action of Nf in DOCA rats may be dependent on the hyperactivity of the sympathetic nervous system and AVP, which facilitates calcium influx, and in the normotensive animals the depressor response to Nf may relate to blockade of the calcium influx, independent of the sympathetic nervous system, AVP and ANG II.

Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure

1992 ◽  
Vol 262 (6) ◽  
pp. E763-E778 ◽  
Author(s):  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blood Pressure Control ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Ang Ii ◽  
Arterial Blood ◽  
Baroreceptor Reflexes ◽  
Sympathetic Nervous

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.

Role of the sympathetic nervous system in the alcohol–guanabenz hemodynamic interaction

1992 ◽  
Vol 70 (9) ◽  
pp. 1217-1224 ◽  
Author(s):  
Abdel A. Abdel-Rahman ◽  
Robert G. Carroll ◽  
Mahmoud M. El-Mas
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Spontaneously Hypertensive Rats ◽  
Specific Interaction ◽  
Plasma Catecholamines ◽  
Hypotensive Effect ◽  
Plasma Catecholamine ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Sympathetic Nervous

The present study evaluated the contribution of the sympathetic nervous system to the adverse hemodynamic action of ethanol on hypotensive responses in conscious unrestrained spontaneously hypertensive rats. Ethanol caused a dose-related attenuation of the hypotensive effect of guanabenz. An equivalent hypotensive response to sodium nitroprusside was not influenced by ethanol, which indicates a potential specific interaction between ethanol and guanabenz. Alternatively, it is possible that a preexisting high sympathetic nervous system activity, which occurred during nitroprusside infusion, may mask a sympathoexcitatory action of ethanol. Further, ethanol (1 g/kg) failed to reverse the hypotensive effect of the ganglionic blocker hexamethonium. This suggests that a centrally mediated sympathoexcitatory action of ethanol is involved, at least partly, in the reversal of hypotension. In addition, the antagonistic interaction between ethanol and guanabenz seems to take place within the central nervous system and involves opposite effects on central sympathetic tone. Finally, changes in plasma catecholamines provide supportive evidence for the involvement of the sympathetic nervous system in this interaction. In a separate group of conscious spontaneously hypertensive rats, ethanol (1 g/kg) reversed the guanabenz-evoked decreases in blood pressure and plasma catecholamine levels. It is concluded that (i) ethanol adversely interacts with centrally acting antihypertensive drugs through a mechanism that involves a directionally opposite effect on sympathetic activity, and (ii) a sympathetically mediated pressor effect of ethanol is enhanced in the presence of an inhibited central sympathetic tone.Key words: spontaneously hypertensive rats, ethanol, catecholamines, guanabenz, hexamethonium.

Chronic antioxidant therapy lowers blood pressure in adult but not in young Dahl salt hypertensive rats: the role of sympathetic nervous system

2013 ◽  
Vol 208 (4) ◽  
pp. 340-349 ◽  
Author(s):  
I. Vaněčková ◽  
M. Vokurková ◽  
H. Rauchová ◽  
Z. Dobešová ◽  
O. Pecháňová ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Antioxidant Therapy ◽  
Hypertensive Rats ◽  
Sympathetic Nervous

scholarly journals Altered Neural and Vascular Mechanisms in Hypertension

2011 ◽  
pp. 381-402 ◽  
Author(s):  
M. PINTÉROVÁ ◽  
J. KUNEŠ ◽  
J. ZICHA
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
G Proteins ◽  
High Blood Pressure ◽  
Calcium Current ◽  
Calcium Influx ◽  
Dominant Role ◽  
Cardiovascular Complications ◽  
Sympathetic Nervous

Essential hypertension is a multifactorial disorder which belongs to the main risk factors responsible for renal and cardiovascular complications. This review is focused on the experimental research of neural and vascular mechanisms involved in the high blood pressure control. The attention is paid to the abnormalities in the regulation of sympathetic nervous system activity and adrenoceptor alterations as well as the changes of membrane and intracellular processes in the vascular smooth muscle cells of spontaneously hypertensive rats. These abnormalities lead to increased vascular tone arising from altered regulation of calcium influx through L-VDCC channels, which has a crucial role for excitation-contraction coupling, as well as for so-called “calcium sensitization” mediated by the RhoA/Rho-kinase pathway. Regulation of both pathways is dependent on the complex interplay of various vasodilator and vasoconstrictor stimuli. Two major antagonistic players in the regulation of blood pressure, i.e. sympathetic nervous system (by stimulation of adrenoceptors coupled to stimulatory and inhibitory G proteins) and nitric oxide (by cGMP signaling pathway), elicit their actions via the control of calcium influx through L-VDCC. However, L-type calcium current can also be regulated by the changes in membrane potential elicited by the activation of potassium channels, the impaired function of which was detected in hypertensive animals. The dominant role of enhanced calcium influx in the pathogenesis of high blood pressure of genetically hypertensive animals is confirmed not only by therapeutic efficacy of calcium antagonists but especially by the absence of hypertension in animals in which L-type calcium current was diminished by pertussis toxin-induced inactivation of inhibitory G proteins. Although there is considerable information on the complex neural and vascular alterations in rats with established hypertension, the detailed description of their appearance during the induction of hypertension is still missing.

Neural and hormonal control of blood pressure in conscious monkeys

1990 ◽  
Vol 258 (1) ◽  
pp. H107-H112
Author(s):  
K. G. Cornish ◽  
M. W. Barazanji ◽  
R. Iaffaldano
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Random Sequence ◽  
Hormonal Control ◽  
Ang Ii ◽  
Controlling Mechanism ◽  
Sympathetic Nervous ◽  
A Minor ◽  
Ganglionic Blocking

The contribution of the autonomic nervous system, angiotensin II (ANG II), and arginine vasopressin (AVP) to the control of blood pressure (BP) was examined in 12 chronically instrumented tethered monkeys. The vasopressin antagonist, [d(CH2)5AVP] (Manning Compound, MC), the ANG II antagonist, saralasin (SAR), and the ganglionic blocking drug, hexamethonium (Hx), were injected in a random sequence into the left atrium (LA) while BP and heart rate (HR) were monitored. When given as the first antagonist, MC caused a slight decrease in BP; SAR did not significantly decrease BP regardless of the sequence of administration, whereas Hx caused a consistent decrease in blood pressure of 35–50 mmHg. Seven (4 intact and 3 with renal denervation) additional animals were involved in hemorrhage experiments. Blood pressure was reduced to 50–60 mmHg by hemorrhage and then allowed to return spontaneously. Ten to 15 min after the end of the hemorrhage, MC was given. When blood pressure had stabilized, SAR was given. Blood pressure returned to 80–90 mmHg after the hemorrhage. MC did not affect the blood pressure recovery; however, saralasin reduced it to the post-hemorrhage levels. We would conclude that the sympathetic nervous system is the primary controlling mechanism for BP in the conscious primate, with AVP making a minor contribution. The release of renin would appear to be primarily under the control of the sympathetic nervous system.

scholarly journals Impaired control of L-type voltage-dependent calcium channels in experimental hypertension

2009 ◽  
pp. S43-S54
Author(s):  
M Pintérová ◽  
S Líšková ◽  
Z Dobešová ◽  
M Behuliak ◽  
J Kuneš ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Cyclic Nucleotides ◽  
Calcium Influx ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Sympathetic Nervous

Blood pressure (BP) level results from the balance of vasoconstrictors (mainly sympathetic nervous system) and vasodilators (predominantly nitric oxide and endothelium-derived hyperpolarizing factor). Most of the forms of experimental hypertension are associated with sympathetic hyperactivity and endothelial dysfunction. It is evident that nitric oxide and norepinephrine are antagonists in the control of calcium influx through L-type voltage-dependent calcium channels (L-VDCC). Their effects on L-VDCC are mediated by cGMP and cAMP, respectively. Nevertheless, it remains to determine whether these cyclic nucleotides have direct effects on L-VDCC or they act through a modulation of calcium-activated K+ and Cl- channels which influence membrane potential. Rats with genetic or salt hypertension are characterized by a relative (but not absolute) NO deficiency compared to the absolute enhancement of sympathetic vasoconstriction. This dysbalance of vasoconstrictor and vasodilator systems in hypertensive animals is reflected by greater calcium influx through L-VDCC susceptible to the inhibition by nifedipine. However, when the modulatory influence of cyclic nucleotides is largely attenuated by simultaneous ganglionic blockade and NO synthase inhibition, BP of spontaneously hypertensive rats remains still elevated compared to normotensive rats due to augmented nifedipine-sensitive BP component. It remains to determine why calcium influx through L-VDCC of hypertensive rats is augmented even in the absence of modulatory influence of major vasoactive systems (sympathetic nervous system, nitric oxide).

Sign in / Sign up

Export Citation Format

Share Document