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PubMed1986

Historical perspective on the management of hypertension.

Remarkable progress has been made during the past 30 years in the management of hypertension, a disease that affects approximately one out of every four adults in the United States. In the 1960s, at least half of the individuals with hypertension were unaware of their disease, and the blood pressures of fewer than 20 percent were controlled at normotensive levels. In contrast, in the 1980s, only a small percentage, perhaps as few as 10 or 15 percent of hypertensive patients, are unaware of their disease and, in many parts of the country, more than 60 percent are being treated to goal blood pressure levels. More effective treatment of hypertension is probably a major reason for the 45 percent decrease in stroke mortality rates in the last 12 years alone and for the dramatic decrease in the number of hypertensive patients in whom renal failure or congestive heart failure develops. In addition, at least a portion of the 25 to 30 percent decrease in coronary mortality rates can probably be attributed to better management of patients with hypertension. The availability of antihypertensive drugs in the 1950s (rauwolfia preparations, veratrum derivatives, thiocyanates, hydralazine, and the ganglion blockers) and the discovery of more effective agents in the period from the 1960s to the present have dramatically improved the prognosis of hypertensive patients. Thiazide diuretics, centrally acting sympatholytic agents, beta-adrenergic inhibitors, and, more recently, selective alpha-adrenergic inhibitors, converting-enzyme inhibitors, and calcium entry blockers are examples of these medications. All of these agents have some side effects, with varying patient acceptability. The search continues for newer drugs that are well tolerated, that lower blood pressure by reducing peripheral resistance, and that produce few metabolic changes. A detailed review of the physiologic effects of antihypertensive medications, as well as a critique of the clinical trials and some of the problems noted in the pharmacologic management of hypertension, is presented.

Adrenergic alpha-Antagonists↗
PubMed1987

Norepinephrine regulation of fetal heart rate: multiple mechanisms of action.

Norepinephrine was infused intravenously for 30 minutes into chronically catheterized sheep fetuses averaging 133 days' gestation. At infusion rates of 3.9, 12, and 39 micrograms/min, heart rate initially decreased as much as 40 bpm and then gradually increased to 50 bpm above the control value by the end of the infusion. Thereafter, heart rate increased further, and by the end of a 30-minute recovery period, heart rate was still 66 bpm above the control value. In fetuses pretreated with either a ganglionic blocker or a parasympathetic blocker, norepinephrine caused a large and sustained rise in heart rate by 124 bpm, which declined rapidly when the infusion was terminated. These results suggest that circulating norepinephrine affects fetal heart rate by several mechanisms: a baroreceptor-mediated suppression, a direct stimulation by norepinephrine, a gradual weakening of the vagal and an increase in cardiac sensitivity to sympathetic stimulation. In addition, there appears to be a long-term positive correlation between fetal heart rate and circulating norepinephrine levels.

Animals↗
PubMed1982

Factors influencing the altered pain perception in the spontaneously hypertensive rat.

Recent studies have demonstrated a hypoalgesia in hypertensive subjects. This study reports and evaluates factors responsible for the expression of the hypoalgesic behavior demonstrated by genetically hypertensive rats of the Okamoto-Aoki strain (SHR) as compared to normotensive age-matched Wistar-Kyoto rats (WKY). Analgesiometric assays were conducted by the hot plate method. SHR's hypoalgesic behavior was reversed by subcutaneously administered naloxone. The intravenous administration of naloxone did not alter arterial pressure or heart rate in either SHR or WKY. Subcutaneous administration of the peripherally acting ganglionic blocker hexamethonium bromide at a dose which lowered mean arterial blood pressure and thus decreased tonic baroreceptor stimulation, concomitantly reversed the SHR hypoalgesic behavior and induced a hyperalgesia in WKY. Denervation of the sino-aortic baroreceptors failed to alter the hypoalgesic behavior demonstrated by SHR. Denervation of the right vagal nerve trunk with associated cardiopulmonary baroreceptor afferents resulted in a reduction of the SHR hypoalgesic behavior and produced a hyperalgesic behavior in WKY as compared to age-matched sham operated controls over a 4 week period. These data suggest a possible physiological role for vagal afferent systems in the concomitant regulation of resting arterial blood pressure and responsiveness to aversive environmental stimuli. A discussion of the interaction between blood pressure and pain regulatory systems as potential substrates associated with the onset and maintenance of hypertension is provided.

Animals↗
PubMed1983

Antianaphylactic effect of naloxone in mice is mediated by increased central sympathetic outflow to sympathetic nerve endings and adrenal medulla.

Intravenous naloxone, 1 or 10 mg/kg, protects sensitized mice from lethal anaphylaxis. The protective effect is reversed by pretreatment with the ganglionic blocker, chlorisondamine chloride, peripheral chemical sympathectomy with 6-hydroxydopamine or bilateral adrenal gland denervation. The possible involvement of the sympathetic nervous system in naloxone's antianaphylactic action, suggested by these findings, is discussed.

Adrenal Medulla↗
PubMed1985

The action of centrally administered arginine vasopressin on blood pressure in the conscious rabbit.

In addition to its peripheral endocrine actions, arginine vasopressin (AVP) has been implicated in the central control of blood pressure. Intracerebroventricular (i.c.v.) injections (0.01-1.0 nmol) of AVP or arginine vasotocin (AVT), but not oxytocin (OXY), into unanesthetized rabbits caused a rapid, dose related rise in blood pressure as well as increases in heart rate. The lowest centrally administered dose of AVP and AVT (0.01 nmol) had no effect on blood pressure when given intravenously. In search of tissue locus for the pressor effect of AVP microinjection of AVP and OXY into the posterior hypothalamus and septum of conscious rabbits was without effect. However, microinjection (0.01-0.04 nmol) of AVP into the nucleus tractus solitarius of anesthetized rabbits caused a rise in blood pressure similar to the response seen after i.c.v. injection. Comparable volumes of the vehicle into the ventricle or the tissue sites had no effect on resting blood pressure. The pressor response after AVP given i.c.v. was significantly reduced up to 3 h after administration of the ganglionic blocker, chlorisondamine HCl. The central antagonist, d(CH2)5Tyr (Me) vasopressin, eliminated the usual increase in blood pressure after administration of AVP in half the animals tested. The results indicate that AVP acts centrally to mediate cardiovascular responses in unanesthetized as well as anesthetized rabbits.

Animals↗
PubMed1985

Beneficial effect of gamma-endorphin-type peptides in anaphylactic shock.

gamma-Endorphin-type peptides (i.e. gamma-endorphin, des-tyr'-gamma-endorphin [DT gamma E]) result from the processing of the opioid peptide, beta-endorphin. Previous studies have implicated the involvement of beta-endorphin in various types of shock, including anaphylactic shock. In the present experiments the intracerebroventricular (i.c.v.) administration of gamma-endorphin (10 micrograms) or DT gamma E (3.3-10 micrograms) significantly improved survival in anaphylactic shock in mice. Moreover, DT gamma E (10 micrograms) reversed the effect of i.c.v. beta-endorphin (3.3 micrograms) to exacerbate shock. A similar dose of DT gamma E was ineffective in antagonizing beta-endorphin-induced analgesia. The anti-anaphylactic action of DT gamma E as well as its effect to block the pro-anaphylactic action of beta-endorphin were prevented by pretreatment with the sympathetic ganglionic blocker, chlorisondamine chloride. The results suggest that gamma-endorphin-type peptides may act in the central nervous system (CNS) to physiologically oppose the autonomic pathophysiologic influences of beta-endorphin.

Anaphylaxis↗
PubMed1989

Cardiovascular effects of substance P receptor stimulation in the ventrolateral medullary pressor and depressor areas.

The pressor (VLPA) and the depressor (VLDA) areas in the ventrolateral medulla were identified with the microinjection of L-glutamate (1.77 nmol/site) in artificially ventilated urethane-anesthetized male Wistar rats. Bilateral microinjection of a stable substance P (SP) agonist [pGlu5, MePhe8, Sar9]-SP(5-11)], abbreviated as DiMe, into the VLPA (6-600 pmol/site) produced a dose-dependent increase in blood pressure (BP). The effects on heart rate (HR) were variable. Intravenous pretreatment with a ganglionic blocker chlorisondamine (3.0 mg/kg, i.v.), but not with a vasopressin antagonist, blocked these responses. Similar microinjection of DiMe (6-600 pmol/site) into the VLDA produced a dose-dependent decrease in HR but had no effect on BP levels. The DiMe-induced bradycardic response elicited from the VLDA was blocked by i.v. pretreatment with atropine methylbromide (0.5 mg/kg, i.v.). These findings indicate that there are SP receptors localized on sympathoexcitatory neurons in the VLPA and that SP may be an excitatory neurotransmitter in this area. In the VLDA, the SP receptors appear to be localized on a subpopulation of neurons that affect vagal, but not sympathetic, outflow to the heart.

Adrenergic Fibers↗
PubMed1989

Facilitation of ACTH secretion by morphine is mediated by activation of CRF releasing neurons and sympathetic neuronal pathways.

Exogenously applied opioid agonists have a stimulatory effect on adrenocorticotropic hormone (ACTH) secretion. The present experiments were designed to examine the mechanisms involved in the stimulatory effect of the mu-receptor agonist morphine on ACTH release in chronically cannulated, freely moving, non-stressed rats. Morphine (7.5 mg/kg, i.v.) treatment was followed by a significant increase in plasma levels of ACTH. Pretreatment with the peripheral ganglionic blocker chlorisondamine (3 mg/kg, i.p.) attenuated the response to morphine. The morphine stimulatory effect was also partially inhibited if the rats were pretreated with a specific antiserum to corticotropin-releasing factor (CRF). In rats given both CRF antiserum and chlorisondamine, the plasma ACTH levels remained unchanged after morphine application. These findings indicate that morphine stimulates the release of ACTH by activating both CRF-secretion and peripheral sympathetic neuronal pathways.

Adrenocorticotropic Hormone↗
PubMed1989

Microinjections of cholinergic agonists into the intermediolateral cell column of the spinal cord at T1-T3 increase heart rate and contractility.

Cardiovascular responses to the microinjections of cholinergic agonists into the intermediolateral cell column (IML) of the spinal cord at T1-T3 level were studied. Mean arterial pressure (MAP), heart rate (HR), the rate of increase in the left ventricular pressure (dp/dt) and contractility index (CI) were monitored in immobilized and artificially ventilated male Wistar rats either anesthetized with pentobarbital or decerebrated at mid-collicular level. Microinjections (20 nl) of carbachol (110-660 pmol) into the right IML elicited a marked increase in HR and a small increase in CI. A marked increase in the CI with relatively little effect on the HR was observed when carbachol was injected into the left IML. The cardioacceleratory effects of carbachol, but not those of L-glutamate, were blocked by prior microinjections of scopolamine (18 nmol) into the IML. Intravenous injections of chlorisondamine (a ganglion blocker) also blocked these effects of carbachol. Spinal transections at C4 or T6 level did not alter these responses. Microinjections of acetylcholine (0.01-1 nmol) into the right IML also produced tachycardic effects. The responses to acetylcholine were blocked by prior injections of a muscarinic receptor blocker (atropine hemisulfate, 0.2 nmol). Microinjections of a selective M2 muscarinic receptor agonist, cis-methyldioxolane (CD; 0.2-0.8 nmol), but not those of a relatively selective M1 receptor agonist (McN-A343; 2-3 nmol), into the right IML elicited an increase in HR. Previous microinjections of a selective competitive M2 receptor antagonist (AFDX-116; 0.8 nmol), but not those of a potent selective M1 receptor antagonist (pirenzepine; 2 nmol), into the IML blocked the effects of CD. Nicotine (0.25-1 nmol) when injected into the right IML also produced positive chronotropic effects. These responses were blocked by prior microinjections of hexamethonium (5 nmol). The above-mentioned results suggest that cholinoceptive neurons, interneurons or terminals are located in the areas of IML which control cardiac functions. Muscarinic as well as nicotinic receptors are present in this area. Muscarinic receptors are predominantly of the M2 type. The physiological significance of the presence of cholinergic receptors in this area in controlling cardiac functions remains to be established.

Acetylcholine↗
PubMed1990

Activation of brown adipose tissue thermogenesis by chemical stimulation of the posterior hypothalamus.

The posterior hypothalamus (PH) is involved in the generation of behavioral thermoregulatory responses, but the importance of the PH in the control of autonomic thermoregulatory responses such as heat production in brown adipose tissue (BAT) is not well defined. In the present study, selective stimulation of PH neurons by local application of the excitatory amino acid glutamate (250 nl of 1 M solution, unilaterally) caused a sharp, transient increase in interscapular BAT (IBAT) and core temperature in urethane-anesthetized rats. This effect was blocked by pretreatment with the sympathetic ganglionic blocker, chlorisondamine chloride (2 mg/kg) or the beta-adrenergic receptor blocker, propranolol (2 mg/kg), implicating the involvement of the sympathetic system. The effect of intra-PH injection of glutamate on IBAT and core temperatures could be mimicked by injection of the gamma-aminobutyric acid (GABA) receptor antagonist, bicucullin methiodide (BMI, 50 ng), into the same PH site. This effect of BMI could be blocked by co-injection of the GABA(A) receptor agonist, muscimol (25 ng). Further, BMI co-injection potentiated the effect of intra-PH injection of glutamate on IBAT and core temperatures. Conversely, muscimol co-injection prevented the stimulatory effect of intra-PH injection of glutamate. Taken together, the results indicate that direct chemical stimulation of neurons in the PH can activate an autonomic mechanism controlling heat production in BAT. Further, they suggest the neural mechanism in the PH mediating this effect is tonically inhibited by GABA, as blockade of GABAergic function in the PH produces an effect similar to that observed after direct stimulation of PH neurons with glutamate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue, Brown↗
PubMed1990

Intra-ventromedial hypothalamic injection of glutamate stimulates brown adipose tissue thermogenesis in the rat.

The ventromedial hypothalamic nucleus (VMH) has been recognized for its role in the control of thermogenesis in brown adipose tissue (BAT) in the rat. However, the neural elements within the VMH that might be involved have not been clearly identified. In the present study, intra-VMH microinjections of the excitatory amino acid glutamate (100 mM to 1 M, in 0.25 microliters), which excites cell bodies and dendrites but not axons and nerve terminals, dose-dependently increased interscapular BAT (IBAT) temperature in urethane-anaesthetized rats. This effect of glutamate was blocked by prior treatment with the sympathetic ganglionic blocker, chlorisondamine chloride (2.5 mg/kg, i.p.) or the beta-adrenergic receptor antagonist, propranolol (2.5 mg/kg, i.p.), implicating the involvement of sympathetic norepinephrine. These results are consistent with the view that cells in the VMH are implicated in the transmission of thermogenic signals to BAT.

Adipose Tissue, Brown↗
PubMed1990

Injection of prostaglandin E2 into the anterior hypothalamic preoptic area activates brown adipose tissue thermogenesis in the rat.

E series prostaglandins (PGE) are known to elicit potent hyperthermia when injected into the anterior hypothalamic preoptic area (POAH) in rats, but the effector mechanisms mediating the rise in temperature are not well defined. In the present study, microinjection of PGE2 into the POAH dose-dependently increased non-shivering thermogenesis in brown adipose tissue (BAT) in urethananesthetized rats, bringing about a marked and sustained rise in interscapular BAT (IBAT) and core temperatures. The effect of intra-POAH PGE2 injection on IBAT and core temperatures could be blocked by systemic pretreatment with the sympathetic ganglionic blocker chlorisondamine chloride or the beta-adrenergic receptor blocker propranolol, thus implicating the involvement of the sympathetic system. Furthermore, the increase in IBAT and core temperatures induced by intra-POAH PGE2 could be blocked by prior injection of the local anesthetic procaine or the GABA receptor agonist muscimol into the ipsilateral ventromedial hypothalamic nucleus (VMH). Taken together, the results suggest that PGE2 increases body temperature by acting in the POAH to stimulate heat production in BAT via a sympathetic efferent mechanism located in the VMH.

Adipose Tissue, Brown↗
PubMed1990

Effects of intrathecal administration of thyrotropin releasing hormone and its analogue, DN1417, on plasma glucose and catecholamine levels in conscious rats.

Effects of intrathecal (i.t.) administration of TRH and the TRH analogue, DN1417, on plasma catecholamines and glucose levels were studied in conscious male rats. The i.t. administration of TRH (0.6 and 3 nmol) at the T8-10 vertebral level resulted in a dose-related increase in epinephrine (E), norepinephrine (NE), and glucose levels, which was suppressed by prior administration of the ganglionic blocker, hexamethonium (1.5 mg/100 g b. wt.). I.t. administration of TRH (3 nmol) caused small increases in plasma E and glucose at the C7-T1 vertebral level, but it did not change plasma E, NE and glucose levels at the sacral level. DN1417 (3 nmol) administered i.t. at the T8-10 or C7-T1 vertebral level had a more potent and long-lasting effect in stimulating the release of E than TRH. These findings suggest that TRH may act on sympathetic preganglionic neurons at the T7-10 spinal levels and stimulate the release of catecholamines from the adrenal medulla.

Animals↗
PubMed1990

Intrathecal administration of delta receptor agonists in the urethane anesthetized rat provokes an increase in arterial pressure via a non-opioid mechanism.

Intrathecal administration of the delta receptor specific agonists Leu5-enkephalin (Leu-Enk; 300 nmol), Met5-enkephalin (Met-Enk; 300 nmol) and [D-Pen2,D-Pen5]enkephalin (DPDPE; 100 nmol) to the T2 or the T9 segment of the rat spinal cord provoked a transient (less than 5 min) increase (15-20 mm Hg) in arterial pressure. DPDPE, but not Leu-Enk or Met-Enk, also significantly increased heart rate by 30-35 bpm. Intravenous administration of 300 nmol of Leu-Enk mimicked the effects observed following intrathecal administration. The hypertensive effect of intrathecal and intravenous Leu-Enk administration was blocked by prior systemic administration (10 mg/kg) of the nicotinic ganglion blocker hexamethonium, suggesting that the effect was mediated via sympathetic activation. The increase in arterial pressure observed following intrathecal Leu-Enk administration was not blocked by either intrathecal (305 nmol) or intravenous (10 mg/kg) administration of the opiate receptor blocker naloxone, although naloxone did block the hypertension provoked by intravenous Leu-Enk administration. Moreover, intrathecal administration of Des-Tyr1-Leu-Enk (300 nmol), an enkephalin fragment devoid of opiate receptor activity, also increased arterial pressure. These results suggest that the hypertension elicited by intrathecal delta agonist administration was not mediated via an opioid mechanism.

Anesthesia↗
PubMed1990

Stimulation of the paraventricular nucleus with glutamate activates interscapular brown adipose tissue thermogenesis in rats.

The paraventricular nucleus (PVN) of the hypothalamus is involved in the control of energy balance in rodents through its influences on feeding, pituitary hormone secretion and the autonomic nervous system. In the present study, selective stimulation of PVN neurons by means of local microinjection of the excitatory amino acid glutamate (100 mM, 500 mM or 100 nl) led to a concentration-dependent increase in interscapular brown adipose tissue (IBAT) temperature in urethane-anaesthetized rats. This effect could be prevented by pretreatment with the sympathetic ganglionic blocker, chlorisondamine chloride, or the beta-adrenergic receptor antagonist, propranolol, but not by hypophysectomy, implicating the involvement of the sympathetic outflow. Thermogenesis in brown adipose tissue (BAT) is an important accompaniment of overfeeding in small mammals, and previous studies have shown that signals generated in response to feeding gain access to the PVN. The present finding that direct activation of PVN neurons stimulates thermogenesis in BAT, taken together with data that the PVN receives dietary signals from the gut, support the view that PVN neurons may function in monitoring the balance between energy intake and its expenditure.

Adipose Tissue, Brown↗
PubMed1991

Activation of brown adipose tissue thermogenesis by chemical stimulation of the hypothalamic supraoptic nucleus.

Glutamate microinjection (1 M, 250 nl) into the hypothalamic supraoptic nucleus (SON) stimulated heat production in brown adipose tissue (BAT) and caused a rapid and sustained increase in interscapular BAT and core temperatures in urethane-anaesthetized rats. This effect was blocked by intraperitoneal pretreatment with a sympathetic ganglionic blocker, chlorisondamine chloride (2.5 mg/kg), or a beta-adrenergic receptor blocker, propranolol (2.5 mg/kg), but not by prior hypophysectomy or intracerebroventricular pretreatment with specific receptor blockers to vasopressin (d(CH2)5[Tyr(Me)2]AVP, 5 micrograms) or oxytocin (d(CH2(5)[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT, 5 micrograms). The results demonstrate that stimulation of SON cells with glutamate elicits a non-vasopressinergic/non-oxytocinergic neural signal that can bring about a sympathetically-mediated increase in BAT thermogenesis. Heat production in BAT is an important mechanism of thermal protection during cold stimulation, and there is evidence that osmotic stimulation can influence thermoregulation. SON neurons play a major role in osmoregulation via release of the peptide hormones vasopressin and oxytocin. The present results suggest the possibility that apart from releasing peptide hormones for osmoregulation, SON neurons might be involved in mediating the effect of osmotic stimulation on thermoregulatory responses involved in thermal adaptation.

Adipose Tissue, Brown↗
PubMed1991

Intrathecal administration of dynorphin A and its fragments increase heart rate and arterial pressure in the urethane anesthetized rat: mediation by a nonopioid mechanism.

Intrathecal administration of 6.50 nmol of dynorphin A (dyn A) (1-13) and (1-17) to the ninth thoracic (T9) spinal segment provoked a transient (5-10 min) increased in heart rate (40-60 beats per minute (bpm] and arterial pressure (20-25 mmHg). Intravenous administration and administration to the second thoracic (T2) segment failed to mimic the effect of T9 administration, suggesting that the cardiovascular effects of T9 administration did not occur via diffusion to the periphery or to the brainstem. The cardioacceleratory and hypertensive responses to T9 dyn A (1-13) administration were prevented by pretreatment with the nicotinic ganglion blocker hexamethonium (10 mg/kg), but were unaffected by bilateral adrenalectomy. These results suggest that the cardiovascular effects of dyn A were mediated predominantly via a sympathetic pathway that does not innervate the adrenal glands. The effects were not antagonized by pretreatment with the opiate receptor antagonist naloxone or by the specific kappa opiate receptor antagonist nor-binaltorphimine, suggesting that they were not mediated via activation of kappa opiate receptors. Further support for this conclusion was provided by experiments demonstrating that dyn A (3-13) (30 nmol), a dynorphin fragment which is devoid of kappa activity, mimicked the effect of dyn A (1-13), whereas administration of the synthetic kappa agonist U50, 488H (100 nmol), failed to elicit effects similar to those provoked by dyn A (1-13). It is concluded that the cardiovascular effects of intrathecal dyn A administration are mediated via a nonopioid mechanism.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1994

Cardiovascular effects of NaCl microinjections into the nucleus of the solitary tract.

The nucleus of the solitary tract (NTS) was systematically explored in the alpha-chloralose-anesthetized rat for sites that elicited changes in mean arterial pressure (MAP) and heart rate (HR) during microinjections (20 nl) of phosphate-buffered saline (PBS; pH 7.2-7.4) or NaCl solutions containing various concentrations of NaCl (104-326 mM). Decreases in MAP (range 7-83 mmHg) and HR (range 10-70 bpm) were consistently elicited from sites in the caudal medial and commissural subnuclei of NTS. Microinjection of PBS or NaCl into other NTS subnuclei or area postrema did not elicit cardiovascular responses. Microinjection of LiCl in PBS elicited cardiovascular responses that were significantly smaller than those elicited by microinjection of NaCl in PBS at the same NTS site. Injections of either a hyperosmotic (400 mOsm/kg) or a hyposmotic (204 mOsm/kg) solution of mannitol into NaCl-sensitive sites did not elicit cardiovascular responses. Finally, most of the sites in NTS that elicited cardiovascular responses during microinjection of glutamate (1 M) did not respond to microinjections of PBS. Administration of atropine methyl bromide had no effect on the magnitude of the depressor response to injections of PBS into NTS, but significantly attenuated (32%) the HR response. Subsequent administration of the ganglionic blockers hexamethonium bromide or arfonad abolished both the depressor and bradycardic responses. These data suggest that within a restricted region of the caudal NTS there exists a pool of neurons sensitive to changes in extracellular Na+ concentrations that, when activated by the sodium, elicit vasodepressor responses as a result of sympathoinhibition and bradycardia as a result of vagal excitation and sympathoinhibition.

Animals↗