Neural Control Of Blood Pressure Research Articles

Increased dietary sodium alters neural control of blood pressure during intravenous ANG II infusion

Increased dietary sodium enhances both excitatory and inhibitory blood pressure responses to stimulation of the central sympathetic nervous system (SNS) centers. In addition, long-term (hours to days) administration of ANG II increases blood pressure by activation of the SNS. These studies investigated the effects of increased dietary sodium on SNS control of blood pressure during 0- to 24-h infusion of ANG II in conscious, male rats consuming either tap water or isotonic saline (Iso) for 2 to 3 wk. The SNS component (evaluated by ganglionic blockade with trimetaphan) of both control blood pressure and the pressor response to intravenous ANG II was reduced in Iso animals. Furthermore, although the pressor response to intravenous ANG II infusion was similar between groups, the baroreflex-induced bradycardia during the initial 6 h of ANG II infusion was significantly greater, whereas the tachycardia accompanying longer infusion periods was significantly attenuated in Iso animals. These data suggest that in normal rats increased dietary sodium enhances sympathoinhibitory responses during intravenous ANG II.

The autonomic nervous system and pressure-natriuresis in cardiovascular-renal interactions in response to salt.

The maintenance of cardiovascular homeostasis represents a balance of activities between of the heart, vascular system and the kidneys in the control of extracellular fluid volume and ultimately blood pressure. Any disturbance in the function of these organs can lead to hypertension and heart failure. Interaction between the cardiovascular and renal systems is exerted dynamically by the autonomic nervous system and humoral factors which together determine the slope of the pressure-natriuresis relationship. This allows the body to ensure that dietary sodium intake can be excreted efficiently without causing major changes in blood pressure. Autonomic control of the kidney is exerted via the renal sympathetic nerves modulating renin release, sodium reabsorption and renal haemodynamics. Epidemiological studies have suggested a weak relationship between the level of dietary sodium intake and the development of hypertension, the underlying mechanisms are uncertain. It is evident from experimental studies that an elevation in dietary sodium intake during the growing phase heightens neural control of blood pressure and the kidney partly due to an enhanced role of the brain renin-angiotensin system. The relationship between dietary sodium and the autonomic regulation of blood pressure and the kidney is increasingly recognised as important but is only poorly understood.

Opioid signalling in the rat rostral ventrolateral medulla.

1. The present article reviews several aspects of opioid signalling in the rostral ventrolateral medulla (RVLM) and their implications for the neural control of blood pressure. 2. In the RVLM, preproenkephalin (PPE) mRNA is expressed by bulbospinal cells that are strongly barosensitive. These putative presympathetic neurons includes C1 and non-C1 neurons. 3. In the RVLM, PPE mRNA is also present in GABAergic neurons that do not project to the thoracic spinal cord. 4. Rostral ventrolateral medulla presympathetic cells receive enkephalinergic inputs and express mu-opioid receptors (MOR). Some of their synaptic inputs also contain MOR. 5. Pre- and post-synaptic modulation of RVLM presympathetic neurons by MOR agonists has been demonstrated in slices of neonate brain. The post-synaptic effect is inhibitory (increased gK). Presynaptic effects include disfacilitation (reduction of glutamate release) and possibly dishinhibition (reduction of GABA release). 6. In conclusion, opioid signalling plays a pervasive role in the medullospinal network that controls sympathetic tone and arterial pressure. Opioid peptides are made by the presympathetic, presumably excitatory, cells of the RVLM and by local GABAergic inhibitory neurons. In addition, RVLM presympathetic neurons are also controlled by opioid peptides at the pre- and post-synaptic level. mu-Opioid receptors are found post-synaptically, whereas presynaptic receptors probably include both mu and delta subtypes. Conditions that trigger the release of opioid peptides by presympathetic neurons or by inputs to these cells are not fully understood and may include decompensated haemorrhage and certain types of peripheral sensory stimulation related to acupuncture.

κ-Opioid receptor antisense oligonucleotide injected into rat hippocampus causes hypertension

Bi-hippocampal microinjection treatment (1 μg per side, twice a day for 5 days) with an antisense phosphorothioate oligodeoxynucleotide antisense oligodeoxynucleotide to the rat κ-opioid receptor, caused hypertension in normotensive Wistar Kyoto (WKY) rats and increased the blood pressure of spontaneously hypertensive rats (SHR). Systolic blood pressure in WKY rats increased from 121±4 to 153±6 mm Hg, and in SHR systolic blood pressure increased from 153±4 to 183±5 mm Hg. Similar results were observed with mean blood pressure, however, there were no changes in heart rate. No significant responses were seen with either vehicle or missense injections. Radioligand binding studies indicated that there was a significant decrease in apparent κ-opioid receptor density due to antisense oligodeoxynucleotide treatment. The results are in accord with our earlier suggestions that the κ-opioid system in the hippocampus may have a role in the neural control of blood pressure.

Antagonist precipitated clonidine withdrawal in rat: Effects on locus coeruleus neurons, sympathetic nerves and cardiovascular parameters

The goal of the present study was to examine the effect of clonidine withdrawal on the neural control of blood pressure. Rats were treated for 7–13 days with clonidine via osmotic minipumps (200 μg kg −1 day −1, s.c.). Controls received saline or were sham operated. Withdrawal was precipitated by the α 2-adrenergic receptor ( α 2-AR) antagonist atipamezole. Most experiments were done under halothane anesthesia. Chronic treatment with clonidine did not change mean arterial pressure (MAP) or heart rate (HR) but raised femoral artery resistance and the activity of locus coeruleus neurons slightly. Atipamezole given to rats treated chronically with clonidine produced the following effects: no change in MAP, severe tachycardia, sustained increase in splanchnic sympathetic nerve discharge (SND; +75±13%), transient increase in lumbar SND (+23±7%), ON–OFF activity pattern in the locus coeruleus (LC). The ON phase of LC activity was synchronized with upswings of SND and with small changes in MAP. A second α 2-AR antagonist, methoxyidazoxan, produced effects identical to those of atipamezole. Atipamezole given to control rats produced no effect on MAP, HR, SND or LC activity. Atipamezole reversed the hypotension, sympathoinhibition and bradycardia produced by acute administration of clonidine. In awake rats treated chronically with clonidine, atipamezole did not change MAP but produced arterial pressure lability and tachycardia. In conclusion, under anesthesia, selective α 2-AR antagonists elicit a clonidine withdrawal syndrome that displays autonomic characteristics reminiscent of the spontaneous withdrawal syndrome found in awake rats. The most prominent features of this syndrome are tachycardia, sympathoactivation, lack of hypertension and an oscillating activity pattern of brainstem neurons leading to abrupt changes in SND and in MAP.

The role of the adrenal medulla in neural control of blood pressure in rats.

The role of the adrenal medulla in the regulation of blood pressure was assessed in rats. In conscious intact (SHAM) and adrenal demedullated (DEMED) animals, baseline blood pressures and heart rates were not different. Moreover, equivalent pressor and depressor response curves to norepinephrine and sodium nitroprusside were obtained. Plasma concentration and 24 hr urinary excretion of norepinephrine were not altered by demedullation. However, epinephrine was undetectable in the urine of the DEMED rats. The effectiveness of the demedullation was further evidenced by a greater than 99% decrease in the epinephrine and norepinephrine content of the adrenal glands of DEMED animals. In pithed SHAM rats, electrical stimulation of preganglionic sympathetic neurons (.5 to 16 hz) elicited marked increases in plasma epinephrine indicating adrenal stimulation, whereas in DEMED rats there were no increases. Furthermore, increments in plasma norepinephrine were significantly reduced in DEMED rats, yet the blood pressure increases were greater than in SHAM rats. Thus, adrenal catecholamine release did not contribute to the blood pressure responses, but in fact, may have had an opposite action due to the vasodilatory actions of epinephrine. The results demonstrate that the adrenal medulla is not essential for reflex compensation to a hypotensive challenge or to the blood pressure increases produced to direct neural stimulation.

Central neural control of blood pressure and cardiac arrhythmias during subarachnoid hemorrhage in rats.

Sudden death may follow subarachnoid hemorrhage which indicates involvement of neural mechanisms connected with the cardiovascular system. Since various regions of the brain mediate blood pressure and heart rate changes, these parameters and heart rhythm could be affected due to a subarachnoid hemorrhage near the circle of Willis which surrounds the hypothalamus, the highest center for autonomic control. To investigate this in the control group, intracranial pressure, blood pressure, and electrocardiogram were measured before and after a simulated subarachnoid hemorrhage; blood pressure and electrocardiogram were measured following midcollicular lesions in the decerebrate group both before and after a subarachnoid hemorrhage. The results demonstrate that an increase in systemic arterial blood pressure and premature ventricular contractions (with respect to unlesioned group, p less than 0.04) are mediated by forebrain areas and require the integrity of neuroanatomical connections with structures that are caudal to the midbrain. Since bradycardia and other electrocardiographic abnormalities could still be produced after midcollicular lesioning it is suggested that they can be mediated via the brainstem only without involvement of more rostral areas and may occur due to increased intracranial pressure.

Australian Neuroscience Society Symposium on “Neural Control of Blood Pressure” Introduction

Australian Neuroscience Society Symposium on “Neural Control of Blood Pressure” Introduction

Control of cardiac output in essential hypertension

Cardiac and renal hemodynamics and cardiopulmonary and total blood volume were determined in 202 men, 101 with normotension and 101 of the same age with chronic essential hypertension, normal renal function and balanced sodium intake and urinary output. Cardiac output was identical in the two groups, whereas blood pressure and total peripheral resistance were significantly different. The two groups exhibited strong differences in the correlation study: (1) Correlations of blood pressure with, respectively, heart rate, cardiopulmonary blood volume and total blood volume were significant in the normotensive group but not in the hypertensive group. (2) Correlations of cardiac output with, respectively, heart rate, cardiopulmonary blood volume and total blood volume were significant in both groups. (3) Correlations of renal blood flow with, respectively, cardiac output, blood pressure and total blood volume were significant in the hypertensive group but not in the normotensive group. This study provides evidence that: (1) the volume and neural control of blood pressure are disrupted in hypertension whereas control of cardiac output is maintained; and (2) adaptive mechanisms involving renal function are necessary to the maintenance of normal cardiac output in patients with essential hypertension.

Adrenolytic and Sympatholytic Actions of Priscol (benzyl-imidazoline)

Summary and ConclusionsPriscol (benzylimidazoline) is sympatholytic as well as adrenolytic in reference to the sympathetic neural control of blood pressure and salivation. Adrenolysis invariably precedes sympatholysis with any dose that is adequate to produce both effects. These pharmacodynamic actions persist during priscol hypotension, pituitrin hypertension and in the presence of atropine.Although sympathetic depression of salivation and vasoconstriction can be produced with variable doses of priscol, up to 15 mg, they are without sympatholytic or adrenolytic effect upon the cervical sympathetic neural components controlling mydriasis, indicating that a differential sympathetic depression characterizes this antisympathetic agent.

A SENSORY CORTICAL REPRESENTATION OF THE VAGUS NERVE: WITH A NOTE ON THE EFFECTS OF LOW BLOOD PRESSURE ON THE CORTICAL ELECTROGRAM

A SENSORY CORTICAL REPRESENTATION OF THE VAGUS NERVE: WITH A NOTE ON THE EFFECTS OF LOW BLOOD PRESSURE ON THE CORTICAL ELECTROGRAM