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

Baroreflex control of heart rate in response to phenylephrine was studied in conscious Sabra hypertension-prone (SBH) rats, at a prehypertensive stage, and hypertension-resistant (SBN) rats. Baroreflex sensitivity as determined from the slope of the relationship of mean arterial blood pressure and heart period was significantly lower in SBH rats (0.58 +/- 0.06 versus 1.71 +/- 0.11 ms/mmHg in SBN rats, P less than 0.01) before the development of hypertension. Sympathetic nerve blockade with guanethidine (15 mg/kg) significantly reduced the slope of the mean arterial blood pressure-heart period relationship in SBN rats to 0.45 +/- 0.05 ms/mmHg (P less than 0.01) and increased the pressor response to phenylephrine, without having any effect on these parameters in SBH rats. Atropine methyl nitrate (1 mg/kg) abolished reflex vagal bradycardia in response to phenylephrine in both groups of rats. This suggests that SBH rats are unable to withdraw the sympathetic cardiac component of the baroreflex in response to a pressor stimulus and appear to rely only on increased vagal activity to effect bradycardia.
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PMID:Sympathetic component of baroreflex control of heart rate is impaired in hypertension-prone (SBH) Sabra rats. 653 May 41

Microinjection of physostigmine (3 micrograms) into the nucleus reticularis dorsalis of the rat produced hypertension. Little or no increases in blood pressure were found at the other areas of the medullary reticular formation. The pressor effect following injection of physostigmine into the nucleus reticularis dorsalis was sensitive to atropine (1 microgram) but resistant to hexamethonium (5 micrograms), similarly injected. Atropine (1 microgram) bilaterally injected into the nucleus decreased pressor responses to intravenous physostigmine (100 micrograms/kg). These data may indicate that there are muscarinic receptors responsible for pressor effects in the nucleus reticularis dorsalis. The medullary cholinoceptors may be involved in the systemic physostigmine effect on blood pressure.
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PMID:The nucleus reticularis dorsalis: a region sensitive to physostigmine. 663 25

Serotonin activates a cardiogenic hypertensive chemoreflex characterized by sudden hypertension. This study in 16 awake and 12 anesthetized dogs was conducted to examine the influence of changes in breathing or heart rate as they may influence the reflex hypertension. In all 28 dogs, either anesthetized or awake, there is a variable but brief initial reflex bradycardia and in all dogs there is transient ventilatory stimulation, but the response in every dog was characterized by hypertension within at most 10 seconds after administering serotonin. Treatment with atropine regularly eliminated the reflex bradycardia and caused the hypertension to appear soon (average of 6 seconds to maximal level). Atropine did not alter the reflex stimulation of breathing. Since atropine eliminated any transient bradycardia (and associated hypertension) but did not prevent reflex changes in breathing, we do not believe that breathing alteration plays any significant hemodynamic role in this reflex.
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PMID:Studies of changes in breathing and blood pressure accompanying a cardiogenic hypertensive chemoreflex compared in conscious and anesthetized dogs. 688 Oct 29

Clonidine poisoning usually causes depressed sensorium, hypotension, and bradycardia. Some patients manifest respiratory depression and miosis simulating narcotic overdose. Supportive care with judicious administration of intravenous fluids, occasionally supplemented by a dopamine infusion, usually reestablished adequate blood pressure. Tolazoline, an alpha-blocker, may reverse clonidine's effects should other efforts fail. Atropine should be used if bradycardia is hemodynamically significant. With massive overdose, clonidine's partial alpha-agonist properties may predominate, resulting in marked hypertension requiring cautious therapy. The experience at Parkland Memorial Hospital with clonidine overdose in six patients demonstrates the myriad of clinical presentations possible.
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PMID:Clonidine overdose: report of six cases and review of the literature. 701 72

Cardiovascular and respiratory effects of intra-left atrial or intra-left ventricular injection of serotonin were studied in conscious dogs (n = 8), anesthetized closed-chest dogs (n = 13) and anesthetized open-chest dogs (n = 9). Serotonin (50-200 microgram), injected as a bolus, resulted in an initial bradycardia and hypotension followed by a delayed tachycardia and hypertension in the conscious dogs. The hypertension was seen as an increase of 21.5 +/- 2.7 (mean +/ SE) mm Hg from a control pressure of 102.5 +/- 1.9 mm Hg, whereas the initial decrease in pressure was 22.6 +/- 1.9 mm Hg. The tachycardia was 23.3 +/- 3.9 beats/min above a control heart rate of 104.9 +/- 3.9 beats/min whereas the bradycardia was 58.5 +/- 3.7 beats/min below control. There was a significant attenuation of the hypotension in both groups of anesthetized dogs. In fact, no hypotension was elicited in the open-chest anesthetized dogs. Open-chest anesthetized dogs showed only a hypertensive response (mean increase 67.2 +/- 5.5 mm Hg). Stimulation of respiration was seen in all groups of dogs. In conscious dogs there was a 214.8 +/- 15.4% increase in respiratory depth and a 20.8 +/- 3.1 breaths/min increase in respiratory rate. Atropine significantly reduced the bradycardia and abolished the hypotension in conscious dogs. Bilateral cervical vagotomy did not abolish the response in open-chest anesthetized dogs. We conclude that the so-called "hypertensive coronary chemoreflex" is altered dramatically by the state of the preparation and by anesthesia.
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PMID:Reflex cardiovascular and respiratory effects of serotonin in conscious and anesthetized dogs. 740 29

It has been suggested previously that norepinephrine does not change fetal placental vascular resistance but does change placental blood flow by changing fetal heart rate. We have tested the hypothesis that fetal heart rate is a determinant of fetal placental blood flow by observing changes in placental vascular resistance in 10 chronically catheterized near-term sheep fetuses. Pressures and flow were observed in the control condition and 150 s after the initiation of infusion of norepinephrine at 50 micrograms/min. The fetuses were then given 1.5 mg of atropine and control observations were again made. The norepinephrine infusion was repeated and pressures and blood flows were measured after 150 s. Atropine increased the fetal heart rate from 168 +/- 6 to 205 +/- 12 beats/min. Placental vascular resistance did not change. Norepinephrine resulted in bradycardia, hypertension and an increased placental vascular resistance. After pretreatment with atropine, norepinephrine resulted in tachycardia, hypertension and an increased placental vascular resistance. We conclude that fetal heart rate is not a major determinant of blood flow and that high doses of norepinephrine cause vasoconstriction of the placental vascular bed of the near-term sheep fetus.
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PMID:Fetal heart rate and umbilical blood flow. 744 Sep 39

Attenuated cholinergic vasodilatation has been suggested as an endothelium-related mechanism involved in essential hypertension. We investigated the role of muscarinic (M) receptor subtypes in the forearm resistance vasculature. In eight white men with essential hypertension and eight matched normotensive control subjects (age of both groups, 47 +/- 4 years; mean +/- SEM), we infused the nonselective agonist methacholine in the presence of saline and the antagonists atropine (nonselective), pirenzepine (M1-selective), and AF-DX 116 (M2-selective) into the brachial artery and measured forearm blood flow and forearm vascular resistance using venous occlusion plethysmography. Affinity constants (pKb values) were determined from calculated plasma concentrations of the infused compounds and EC50 values. Sodium nitroprusside was given as an endothelium-independent control, and minimal forearm vascular resistance after 10 minutes of ischemia was used as a marker of structural vascular changes. Hypertensive patients showed higher minimal forearm vascular resistance, indicating structural vascular changes. However, sodium nitro-prusside- and methacholine-induced vasodilatation was similar in both groups, with apparent EC50 values (log moles per liter; mean +/- SEM) of -7.32 +/- 0.13 and -7.51 +/- 0.21 in hypertensive patients and -7.37 +/- 0.13 and -7.45 +/- 0.02 in control subjects, respectively. Atropine, pirenzepine, and AF-DX 116 caused a shift to the right of the concentration-response curve of methacholine, with apparent pKb values of 8.63 +/- 0.08, 6.81 +/- 0.13, and 5.51 +/- 0.29 in hypertensive individuals and 8.62 +/- 0.10, 6.98 +/- 0.08, and 5.49 +/- 0.09 in control subjects, respectively. Again, there were no statistically significant differences in these pharmacological parameters between hypertensive patients and normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Jul
PMID:In vivo characterization of muscarinic receptor subtypes that mediate vasodilatation in patients with essential hypertension. 760 35

We compared two methods of assessment of baroreflex sensitivity in eight supine healthy volunteers during repeated baseline measurements and various conditions of cardiac autonomic blockade. The spontaneous baroreflex method involved computer scanning of recordings of continuous finger arterial pressure and electrocardiogram to locate sequences of three or more beats in which pressure spontaneously increased or decreased, with parallel changes in pulse intervals. The mean regression slope of all these sequences during each study condition was considered to represent the mean spontaneous baroreflex slope. In the drug-induced method, sigmoidal curves were constructed from data obtained by bolus injections of phenylephrine and nitroprusside; the tangents taken at the resting pressure of each of these curves were compared with the mean spontaneous baroreflex slopes. The two methods yielded slopes that were highly correlated (r = .96, P < .001), with significant but similar intraindividual baseline variability. Atropine virtually eliminated the baroreflex slope; subsequent addition of propranolol did not alter it further. Propranolol or clonidine alone increased average baroreflex slope to the extent that they increased resting pulse interval (r = .69 to .83). The spontaneous baroreflex method provides a reliable, noninvasive assessment of human vagal cardiac baroreflex sensitivity within its physiological operating range.
Hypertension 1995 May
PMID:Spontaneous cardiac baroreflex in humans. Comparison with drug-induced responses. 773 17

Gou-teng is a drug used for treatment of hypertension in Chinese medicine. Its antihypertensive action has been previously confirmed in the spontaneously hypertensive rat (SHR). Here, its vasorelaxing effect and the mechanisms of actions were studied in vitro. Gou-teng extract (GTE) relaxed the norepinephrine (NE)-precontracted aortic ring preparations isolated from Wistar Kyoto rats (WKY) with and without intact endothelium; the latter was significantly less sensitive than the former. The GTE-induced endothelium-dependent relaxation was significantly inhibited by NG-monomethyl-L-arginine (NMMA) in a dose-dependent manner while indomethacin did not affect the relaxation. Atropine inhibited the acetylcholine (ACh)-induced endothelium-dependent relaxation but did not the GTE-induced one. Furthermore, once GTE was applied, the following NE-induced contraction was significantly reduced even after repeated washout. NMMA effectively reduced and rather reversed this residual effect of GTE. From these results, it is concluded that GTE relaxes the NE-precontracted rat aorta through endothelium-dependent and, to lesser extent, -independent mechanisms. The endothelium-dependent component would be mediated by EDRF/NO pathway in which the muscarinic cholinoceptors were not involved. Thus, GTE appears to be a potent and long-lasting vasodilator mainly through EDRF/NO release.
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PMID:Gou-teng (from Uncaria rhynchophylla Miquel)-induced endothelium-dependent and -independent relaxations in the isolated rat aorta. 820 63

The present study examined the time course of changes in baroreceptor reflex function by means of sigmoidal curve-fitting analysis in conscious, unrestrained renovascular one-kidney, one clip (1K1C) rats at 1, 3, 7, 15, 30, and 60 days after renal artery clipping. The reflex heart rate responses were elicited by alternate intravenous bolus injections of phenylephrine (change, +5 to +50 mm Hg) and sodium nitroprusside (change, -5 to -50 mmHg). Atropine methylnitrate and atenolol were given to evaluate the responses mediated by the cardiac sympathetic or vagal component, respectively. The average baroreceptor reflex gain (sensitivity) decreased progressively (day 1, 3.35 +/- 0.3 beats per minute [bpm] per millimeter of mercury), reaching a maximal attenuation in the 30-day 1K1C group (1.83 +/- 0.5 bpm/mm Hg) compared with sham rats (approximately 4.60 bpm/mm Hg). The data showed a decreased vagal activity contributing to the attenuation of the baroreceptor gain only in the 30-day 1K1C group. In contrast, the cardiac sympathetic component of the baroreceptor reflex was significantly decreased in all 1K1C groups (from 2.10 +/- 0.4 to 0.50 +/- 0.2 bpm/mm Hg) compared with the respective sham groups (from 3.80 +/- 0.3 to 3.10 +/- 0.4 bpm/mm Hg). These results suggest that a reduced contribution of the sympathetic component to the baroreceptor heart rate reflex may be the main cause of the progressive attenuation of the baroreceptor reflex sensitivity observed in conscious 1K1C hypertensive rats.
Hypertension 1994 Jan
PMID:Time course of changes in sigmoidal-fitting baroreceptor curves in one-kidney, one clip hypertensive rats. 828 82


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