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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Autoregulation of blood flow in various organ systems is a well-documented phenomenon. However, the net effect of these regional autoregulatory responses on the systemic circulation has not been studied in conscious rats despite the now extensive use of rats in cardiovascular research. The ability of the systemic circulation to autoregulate cardiac output has been proposed to play an important role in the development of increased vascular resistance in volume-dependent forms of hypertension. To better understand these events, we characterized responses to acute increases and decreases in blood volume in conscious areflexic rats that were chronically instrumented with arterial and venous catheters and an electromagnetic flow probe around the ascending aorta. Neurohumoral blockade was achieved with chlorisondamine (10 mg/kg), methscopolamine (0.5 mg/kg), captopril (1.0 mg/kg), and d(CH2)5Tyr(Me)arginine vasopressin (10 micrograms/kg). Mean arterial pressure was restored to normal levels with a constant i.v. norepinephrine infusion, which resulted in normal values of cardiac output, total peripheral resistance, and blood gases. Blood volume expansion (0.9 ml i.v. blood infusion for 6 minutes) increased cardiac output 9 +/- 1% and mean arterial pressure 30 +/- 3% and caused a 22 +/- 2% increase in total peripheral resistance (n = 7). Blood volume contraction (6-minute withdrawal of 0.9 ml of blood) decreased cardiac output 12 +/- 1% and mean arterial pressure 26 +/- 4%, which resulted in a 16 +/- 4% decrease in total peripheral resistance (n = 8). The slopes of the pressure-flow relationships during volume expansion were 0.24 and 0.41 during volume contraction, as compared with a nonautoregulating system (slope = 1) and a completely autoregulating system (slope = 0).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 Jun
PMID:Autoregulation of the systemic circulation in conscious rats. 313 5

Changes in brain neuropeptide content in spontaneously hypertensive rats may be primarily related to the development of hypertension or may be secondary consequences of it. We have measured brain concentrations of beta-endorphin, Leu-enkephalin, arginine vasopressin (AVP) and oxytocin (OXT) in stroke-prone spontaneously hypertensive rats (SHRSP) and in age-matched normotensive Wistar Kyoto (WKY) controls, as well as in SHRSP with normalized blood pressure by chronic treatment with clonidine. Opioid peptide contents were measured in 12-, 18- and 24-week-old rats. beta-Endorphin was measured in the neuro-intermediate and anterior lobes of the pituitary, the hypothalamus, mid-brain and brain stem; Leu-enkephalin in the neuro-intermediate lobe of the pituitary, hypothalamus, mid-brain, brain stem, as well as in the spinal cord and adrenal glands. AVP and OXT were measured in the neuro-intermediate lobe of the pituitary, hypothalamus, brain stem and spinal cord. beta-Endorphin in the neuro-intermediate lobe of the pituitary was significantly higher in 12- and 18-week-old SHRSP. Adrenal gland Leu-enkephalin was lower in SHRSP as compared with the WKY. OXT and AVP contents were markedly reduced in all brain regions of SHRSP except the neuro-intermediate lobe of the pituitary, where no significant changes were found. In no case did long-term antihypertensive treatment with clonidine reverse the altered peptide content in the SHRSP. We conclude that alterations in brain neuropeptide content in SHRSP are not secondary to hypertension. The blood pressure lowering activity of clonidine appears not to depend on major alterations of peptide concentrations. A genetic defect in the synthesis of adrenal enkephalins and hypothalamic OXT and AVP seems likely from these studies.
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PMID:Altered neuropeptide concentrations in spontaneously hypertensive rats: cause or consequence? 315 51

The inhibitory effect of high and low molecular weight native and synthetic rat atrial peptides on oxygen consumption in isolated rat kidney mitochondria and slices was measured. Oxygen consumption by mitochondria was measured in the presence of succinate and/or adenosine diphosphate, furosemide, and low and high molecular weight native and synthetic rat atrial peptides. After the addition of succinate, adenosine diphosphate limiting respiration (State 4) increased in the presence of low, but not high, molecular weight native rat atrial peptides. Furosemide caused a significant decrease in State 4 respiration (p less than 0.001). Angiotensin II and arginine vasopressin did not alter State 4 respiration. The rate of oxygen consumption after the addition of saturating adenosine diphosphate in the presence of saturating succinate (State 3 respiration) was reduced by low and high molecular weight native rat atrial peptides. Furosemide completely blocked oxygen consumption after the addition of adenosine diphosphate. Oxygen consumption was unchanged by trypsin treated (natriuretically inactive) low molecular weight rat atrial peptides and ventricular protein extracts of high and low molecular weight native rat atrial peptides. Synthetic and low molecular weight native rat atrial peptides had similar effects on mitochondrial oxygen consumption. Low molecular weight native and synthetic rat atrial peptides decreased the adenosine diphosphate to oxygen ratio, and these peptides, as well as furosemide, also induced mitochondrial swelling; none of the other rat atrial peptide combinations nor angiotensin II produced this effect. In kidney slices, basal oxygen consumption (without substrates) was stimulated by succinate.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Rat atrial natriuretic peptides inhibit oxygen consumption by rat kidney. 315 63

The cerebrospinal fluid (CSF) concentrations of arginine vasopressin (AVP) and oxytocin (OT) were investigated both in patients with benign intracranial hypertension and in age and sex matched controls. Twenty eight lumbar punctures were performed on 15 patients with benign intracranial hypertension as part of their routine investigation and therapy. All patients had raised intracranial pressure (27.4, SE 1.7 cm.CSF). CSF AVP levels were significantly elevated in benign intracranial hypertension (2.1, SE 0.3 pmol/l) compared with controls (0.7, SE 0.1 pmol/l, p less than 0.001) but CSF OT concentrations were similar in both groups. CSF osmolality and plasma AVP and osmolality were identical in patients and controls. There was no correlation between CSF AVP concentration and intracranial pressure. The selective elevation of AVP in CSF may be of importance in the pathogenesis of raised intracranial pressure in benign intracranial hypertension.
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PMID:Cerebrospinal fluid neurohypophysial peptides in benign intracranial hypertension. 322 Dec 20

We examined the interrelationships between the pressor response to the administration of norepinephrine and arginine vasopressin and baroreflex function in rats with hypertension of two days' duration induced by heminephrectomy and a clip placed on the right renal artery (2-day clipped rats). Mean arterial pressure was higher in the 2-day clipped rats than in heminephrectomized rats without clips (sham-operated rats). The pressor response in the 2-day clipped rats to both agents increased as compared to the sham-operated rats. This hyperresponsiveness was attenuated by administering an angiotensin II antagonist, [1-Sar, 8-Ile] angiotensin II. Baroreflex sensitivity was studied by measuring changes in arterial pressure and pulse interval in response to the injection of phenylephrine. Baroreflex sensitivity was not decreased but markedly increased in the 2-day clipped rats and unaffected by infusing the angiotensin II antagonist. These results provide evidence that 1) in the 2-day clipped rats there are exaggerated pressor responses to vasoconstrictors; 2) the hyperresponsiveness is not causally related to the change of baroreflex sensitivity; and 3) angiotensin II plays a significant role in the increased pressor responses; however, the baroreflex mechanism is not involved in attenuation of the hyperresponsiveness by the angiotensin II antagonist.
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PMID:Role of baroreflex in the pressor response of rats with hypertension developed by renal artery stenosis. 333 54

The present study was undertaken to determine the specificity of the vasoconstrictor activity to angiotensin II (AII) and arginine vasopressin (AVP) on the microcirculation in normal and renovascular hypertensive states. Ten to fourteen days after the induction of hypertension, Syrian hamsters were anesthetized with pentobarbital sodium, the cheek pouch was exposed, and a plastic chamber was placed in situ so the membrane could be suffused with bicarbonate-buffered Ringer's solution (5% CO2, 95% N2, pH 7.4). Third order arterioles (30-45 micron) were identified for study and vessel diameter was measured using a shearing device. In one group of normotensive and hypertensive hamsters, AII was microapplied to the arteriole before and after adding an AVP antagonist to the suffusate. In a second group of similar hamsters, AVP was microapplied to the arteriole before and after adding an angiotensin II blocker, saralasin acetate, to the suffusate. AVP and AII receptor blockade was documented by observing whether the vasoconstrictor effect of either AVP or AII was abolished. Dose-response curves for either peptide were not altered in the presence of the antagonist to the other peptide; however, they were shifted to the left in the RHT hamsters. Neither AVP nor AII receptor blockade altered control resting arteriolar diameters. Thus, it can be concluded that the microvascular response to both AII and AVP are potentiated in RHT and there are no interactions between either AII or AVP with the receptors of the other peptide in these microvessels in normal or RHT hamsters, indicating a high specificity for each peptide to its vascular receptor.
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PMID:Specificity of arginine vasopressin and angiotensin II for microvessels in the hamster cheek pouch after the induction of renovascular hypertension. 334 41

Data from conscious rats, dogs, and humans show that plasma arginine vasopressin (AVP) begins to exert vasoconstrictor activity at concentrations in the same range as those associated with maximum antidiuretic activity. Minimum pressor responses are observed with elevated plasma AVP, due in part to decreases of cardiac output and in part to withdrawal of sympathetic neural tone to various regions of the systemic circulation. These responses appear to some extent to be species-dependent. In conscious dogs, but not in rats, the fall of cardiac output is mediated by AVP stimulation of baroreceptor reflex pathways. Studies in rats indicate that AVP inhibits the sympathetic nervous system by direct action on the central nervous system. No evidence was found for inhibition at peripheral sites such as autonomic ganglia or vascular smooth muscle receptors. Also, AVP plays an important role in the regulation of arterial pressure with blood loss by direct vasoconstriction and by AVP enhancement of the strength of the baroreceptor reflex responses. The role of AVP in the long-term control of arterial pressure and in hypertension remains controversial, but plasma AVP is elevated in many experimental and human forms of hypertension. The link between plasma AVP and hypertension remains unclear because long-term elevation of AVP alone cannot sustain volume expansion or hypertension, and excess AVP does not enhance hypertension produced by sodium-retaining hormones or other vasoconstrictor agents. It appears that AVP plays mainly a permissive role by its fluid-retaining effects in most forms of hypertension. It is also possible that it acts as a central nervous system neural transmitter and modifies autonomic pathways in some forms of hypertension.
Hypertension 1988 Feb
PMID:Vasopressin and arterial pressure regulation. Special lecture. 334 62

Our previous finding that dexamethasone-induced hypertension in rats is associated with enhanced reactivity of mesenteric arteries to arginine vasopressin but not to angiotensin II (Ang II) or norepinephrine has led us to postulate that vasopressin contributes to the development or maintenance of glucocorticoid-induced hypertension. To test this view, we investigated the effects of vasopressin, Ang II, norepinephrine, and the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP on mean arterial blood pressure and heart rate with and without ganglionic blockade with hexamethonium and angiotensin I (Ang I) converting enzyme inhibition with MK 421 in pentobarbital-anesthetized rats made hypertensive by treatment with dexamethasone (1.8 mg/kg/wk for 14 days). Administration of vasopressin, Ang II, or norepinephrine (0.003-3 microgram i.v.) produced a dose-related increase in arterial blood pressure. The pressor response to vasopressin, but not to Ang II or norepinephrine, was greater in dexamethasone-treated than in vehicle-treated animals, and this difference became more pronounced in rats that received hexamethonium and MK 421. Administration of the vasopressin V1 receptor antagonist d(CH2)5Tyr(Me)AVP significantly reduced arterial pressure in dexamethasone-treated but not in vehicle-treated animals. Hexamethonium and MK 421 reduced arterial blood pressure in dexamethasone-treated as well as in vehicle-treated rats; however, arterial blood pressure remained higher in the former. Administration of the vasopressin V1 receptor antagonist produced a greater reduction in arterial blood pressure in dexamethasone-treated than in vehicle-treated rats. These data suggest that vasopressin contributes to glucocorticoid-induced hypertension, which is probably due to enhanced vascular reactivity to the peptide.
Hypertension 1988 Feb
PMID:Contribution of vasopressin in dexamethasone-induced hypertension in rats. 334 65

To determine whether the central vasopressinergic system at the level of nucleus tractus solitarii (NTS) modulates the reflex control of heart rate, we employed a new method for microinjection into the brainstem of conscious, freely moving rats. Baroreceptor reflex function was assessed during pressure changes induced by intravenous administration of phenylephrine (0.25-8 micrograms/kg) and sodium nitroprusside (0.5-16 micrograms/kg) in rats microinjected, through a permanent cannula into the brainstem, with saline, arginine vasopressin (AVP), or an AVP blocker. Baseline levels of pressure and heart rate were not changed by either peptide pretreatment. Restricted injection of AVP (20 ng-0.2 microliter) into the NTS attenuated the reflex bradycardia during pressure increases, with an upward displacement of the baroreceptor reflex function line (p less than 0.01) without change in the sensitivity. Local blockade of endogenous AVP, d(CH2)5Tyr(Me)AVP (1 microgram-0.2 microliter), depressed baroreceptor reflex sensitivity with intense bradycardia to either small or large pressure increases. Baroreceptor reflex control of heart rate in response to decreases in pressure was preserved during pretreatment with AVP, whereas endogenous blockade of AVP increased baroreceptor reflex sensitivity. These effects were specific to the NTS, since in another four rats there were no effects when the injections were made 1 mm above, into the cerebellum. The changes in baroreceptor reflex control of heart rate in conscious, unrestrained rats caused by administration of AVP and its endogenous blockade provide evidence that central vasopressinergic synapses at the NTS are important physiological modulators of baroreceptor reflex function.
Hypertension 1988 Feb
PMID:Baroreceptor reflex modulation by vasopressin microinjected into the nucleus tractus solitarii of conscious rats. 334 66

Angiotensin II (A-II) has been shown to stimulate plasma arginine vasopressin (AVP) secretion in experimental animals, although offsetting effects from a rise in arterial pressure may obscure the effect. A rise in plasma norepinephrine (NE) may have several effects on plasma AVP because of changes in arterial pressure and central adrenergic stimulation. As little data exist concerning these neurohumoral interrelationships in humans, the current investigation was performed to examine the role of acute changes in plasma NE and A-II in the control of arginine vasopressin (AVP). The question is of potential importance because of diffuse disturbances in neurohumoral control in diseases such as hypertension and congestive heart failure. We measured heart rate, arterial pressure, and plasma AVP during 2.5 and 5.0 micrograms/min infusions of NE, and during .05 and .10 micrograms/kg/min infusions of A-II. NE increased mean blood pressure from 81 +/- 11 mm Hg to 87 +/- 16 mm Hg at 2.5 micrograms/min and to 93 +/- 16 mm Hg at 5.0 micrograms/min (p less than .001). Heart rate was unchanged during the 2.5 micrograms/min infusion but declined from 58 +/- 9 beats/min to 54 +/- 9 beats/min during the 5.0 micrograms/min infusion (p = NS). Plasma AVP, 3.0 +/- 0.9 pg/mL, did not change. During A-II infusions, mean arterial pressure increased from 81 +/- 13 mm Hg to 92 +/- 17 mm Hg and 112 +/- 21 mm Hg at the two rates (p less than .001); heart rate declined from 61 +/- 6.8 beats/min to 59 +/- 9.1 beats/min and 56 +/- 11.3 beats/min (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of infused norepinephrine and angiotensin-II on vasopressin levels in humans. 338 90


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