Arterial Plasma Norepinephrine Research Articles

Diagnostic Dosages of Protirelin (TRH) Elevate BP by Noncatecholamine Mechanisms

While performing thyroid function tests, we noticed that protirelin (TRH) raised BP, and, therefore, we investigated the effect of diagnostic dosages of protirelin (500 micrograms) on plasma catecholamine levels and cardiovascular function in eight patients one day before, one day after, and four weeks following heart surgery. Mean arterial pressure (MAP), heart rate (HR), plasma norepinephrine (NE), epinephrine (EPI), dopamine (DA), thyroid hormone (triiodothyronine [T3], thyroxine), and thyrotropin (TSH) levels were measured before and after the intravenous injection of protirelin. Protirelin increased MAP transiently from 88 +/- 2 to 103 +/- 3 mm Hg (before surgery), 86 +/- 4 to 102 +/- 4 mm Hg (one day after surgery), and 86 +/- 4 to 104 +/- 5 mm Hg (four weeks after surgery). There were no notable changes in HR or plasma NE, EPI, or DA levels. The T3 and TSH response to protirelin was normal on all three study days. Protirelin raised MAP by an effect on systemic vascular resistance (SVR) rather than an increase in cardiac output. We conclude the following: (1) diagnostic dosages of protirelin transiently elevate MAP and SVR by a noncatecholamine mechanism, (2) clinicians who perform protirelin tests should be aware of protirelin's transient pressor effects.

Increased peripheral catecholamine release in patients with long-standing, untreated essential hypertension.

Both arterial and venous plasma adrenaline and noradrenaline concentrations were elevated in 20 middle-aged men with long-standing, untreated essential hypertension compared to 19 normotensive control men (p less than 0.01). The mean a-v (arterial-venous) difference of adrenaline and v-a difference of noradrenaline were increased in the hypertensive (p less than 0.05) consistent with raised adrenal adrenaline release and release of noradrenaline from the peripheral vascular beds of the forearm.

Cardiovascular and catecholamine responses to successive episodes of hypoxemia in the fetus.

The cardiovascular and plasma catecholamine responses to successive episodes of hypoxemia were evaluated in 5 fetal lambs in utero (greater than or equal to 0.7 gestation). Fetal heart rate (HR) and blood pressure (BP) were monitored continuously and specimens obtained for arterial blood gases, plasma norepinephrine (NE) and epinephrine (E) during a baseline control period, during each of 5 hypoxemic episodes and during 4 intervening recovery periods. Hypoxemia (PO2 = 9.8-13.7 Torr) was produced by gradual, controlled constriction of the umbilical cord by a silicone rubber cuff. HR fell from 176 +/- 9 beats/min (means +/- SE) to between 105 +/- 11 and 119 +/- 5 (p less than 0.01) and BP increased from 71 +/- 2/49 +/- 1 mm Hg to between 79 +/- 2/55 +/- 2 and 90 +/- 3/66 +/- 3 (p less than 0.01) during the hypoxic periods. There was no evidence of waning in the magnitude of the hypertensive response over the course of successive hypoxemic episodes. Baseline plasma NE and E rose from 278 +/- 65 and 28 +/- 8 pg/ml, respectively, to between a mean of 4,982 and 17,060 pg/ml for NE and 2,217 to 9,471 pg/ml for E. No attenuation in the rise of NE and E was observed throughout the 5 hypoxic periods. Thus, the late gestation fetus appears capable of sustaining appropriate cardiovascular and catecholamine responses to multiple successive episodes of hypoxemia.

Neurohumorally induced cardiac dysrhythmias during nitrous oxide-oxygen-thiopental anesthesia

Barbiturate, nitrous oxide, and oxygen are commonly used by the oral and maxillofacial surgeon to anesthetize the ambulatory oral surgery patient. The authors report three cases of ventricular dysrhythmia occurring from surgical stimulation during nitrous oxide-oxygen-thiopental anesthesia. These dysrhythmias were most likely mediated via direct neural stimulation of cardiac sympathetic nerves. Concomitant with adrenergic stimulation, a rise in the arterial plasma norepinephrine level was documented, along with an increase in the rate-pressure product. Immediate recognition and treatment of ventricular dysrhythmia is mandatory to preclude further serious cardiovascular complications or death.

Influence of circulating NE and Epi on adipose tissue vascular resistance and lipolysis in humans.

The effects of circulating norepinephrine (NE) and epinephrine (Epi) on vascular resistance in subcutaneous adipose tissue and the calf as well as on plasma glycerol, an indicator of lipolysis, were studied in healthy volunteers. Adipose tissue blood flow was determined by the local clearance of 99mTcO-4 or 133Xe. The two isotopes gave similar results. Calf blood flow was determined by venous occlusion plethysmography. Intravenous infusion of NE caused increases in systolic and diastolic blood pressures, adipose tissue and calf vascular resistances, and plasma glycerol and a decrease in plasma insulin and heart rate, all of which were significant when arterial plasma NE was elevated from 1.17 +/- 0.14 to 8.38 +/- 0.30 nM (n = 16). Epi reduced diastolic and mean arterial pressures and adipose tissue and calf vascular resistances and increased plasma glycerol without affecting systolic blood pressure or plasma insulin. An increase of arterial plasma Epi from 0.20 +/- 0.03 to 1.15 +/- 0.05 nM (n = 6) was sufficient to induce vasodilatation in adipose tissue and lipolysis. Human adipose tissue differs from canine adipose tissue inasmuch as Epi causes vasodilatation in humans (present results) but vasoconstriction in the dog (previous results), presumably due to a predominance of vascular beta 2-adrenoceptors in human and beta 1-adrenoceptors in canine adipose tissue. Furthermore, Epi is a considerably more potent lipolytic hormone than NE in humans but not in the dog. Our results indicate that both NE and Epi may influence human adipose tissue blood flow and lipolysis as circulating hormones.

Arterial baroreflex sensitivity, plasma catecholamines, and pressor responsiveness in essential hypertension.

Arterial baroreflex sensitivity, plasma norepinephrine (NE) and epinephrine (E), and pressor and depressor responses were assessed in 25 patients with essential hypertension and 29 normotensive control subjects. Sensitivity of the cardiac limb of the baroreflex was determined by blood pressure and interbeat interval responses associated with the Valsalva maneuver, externally applied neck suction and pressure, and injection of phenylephrine and nitroglycerin. By all these techniques, patients with essential hypertension had significantly decreased baroreflex sensitivity, even after adjustment for age mismatching between the hypertensive and normotensive groups. Hypertensive patients also had significantly higher mean levels of plasma NE and E in both brachial arterial and antecubital venous blood (246 vs 154 pg/ml arterial NE, 286 vs 184 pg/ml venous NE, 99 vs 55 pg/ml arterial E, and 65 vs 35 pg/ml venous E) and significantly larger pressor responses to injected phenylephrine (30.9 mm Hg/100 micrograms vs 16.7 mm Hg/100 micrograms). When baroreflex-cardiac sensitivity values measured by the various techniques were averaged, there was a significant inverse relationship between sensitivity and venous NE and between sensitivity and pressor responsiveness. The results indicate that decreased baroreflex-cardiac sensitivity, increased sympathetic outflow, and pressor hyperresponsiveness tend to occur together in some patients with essential hypertension. Decreased arterial distensibility and altered central neural integration can account for these findings.

METOPROLOL, FENTANYL AND STRESS RESPONSES TO MICROLARYNGOSCOPY: Effects on arterial pressure, heart rate and plasma concentrations of catecholamines, ACTH and cortisol

Forty patients undergoing microlaryngoscopy were anaesthetized with thiopentone and nitrous oxide. Twenty patients received metoprolol 200 mg in a slow-release tablet once daily for 4 days up to, and including, the morning of operation, and 10 mg i.v. shortly before induction of anaesthesia. The other patients received placebo tablets and physiological saline i.v., instead. Both groups of 20 patients were further subdivided, half of the patients receiving fentanyl 1.0-1.5 mg during anaesthesia, the effect of which was antagonized by naloxone at the end of the procedure. The other patients received saline i.v. instead of fentanyl or naloxone. Metoprolol decreased heart rate and the general level of arterial pressure during anaesthesia, but did not affect the fluctuations in pressure. Arterial plasma noradrenaline concentrations during microlaryngoscopy were enhanced by metoprolol, in comparison with placebo, the reverse being the case for cortisol concentrations. Fentanyl decreased arterial pressure and plasma ACTH and cortisol concentrations regardless of whether the patient had received metoprolol. Plasma adrenaline and noradrenaline concentrations were decreased by fentanyl in the patients receiving metoprolol.

Fetal Catecholamine Release in Response to Labor and Delivery

Umbilical arterial plasma norepinephrine and epinephrine were measured using a sensitive, specific radioenzymatic assay. Plasma catecholamines were correlated with umbilical arterial blood gases, durations of the first and second stages of labor, duration of rupture of the membranes, fetal heart rate tracings, and fetal sex. Significant correlations were observed for plasma norepinephrine versus fetal pH and PO2 and plasma epinephrine versus pH but not PO2. The majority of the fetal heart rate tracings demonstrated either a normal baseline or mild variable decelerations. The plasma catecholamines and blood gases were similar in these 2 groups. Significant elevations of both plasma catecholamines were observed with those tracings commonly associated with fetal distress; however, the number of infants was small. No sex differences were observed in plasma norepinephrine or epinephrine or in responsiveness. The results suggest that the human fetus at term responds to acidosis and hypoxia with a graded catecholamine release. This may be an important adaptive mechanism.

Adrenalectomy inhibits noradrenergic, adrenergic, and vasopressor responses to angiotensin II in the Pekin duck (Anas platyrhynchos).

The iv injection of Asp1, Val5-angiotensin II(AII) was followed by increases in arterial plasma norepinephrine (NE) and epinephrine (E) concentrations and elevation of arterial blood pressure in the anesthetized Pekin duck. AII injection did not affect the concentration of unconjugated dopamine in arterial plasma. Adrenalectomy inhibited the increases in plasma NE and E concentrations elicited by AII. Pressor responses to AII also were diminished after adrenalectomy, whereas pressor responses to exogenous NE and tyramine were not measurably affected. The alpha-adrenergic blocking drug phenoxybenzamine diminished the pressor effect of AII in both shamoperated and adrenalectomized ducks. The blockade of alpha-adrenergic receptors by phenoxybenzamine was incomplete, since pressor responses to exogenous NE were lessened by not abolished. We conclude from these experiments that AII increases arterial blood pressure in the Pekin duck by mobilizing NE and E from both adrenal and extraadrenal stores. It remains unknown whether the residual pressor response to AII in phenoxybenzamine-treated, adrenalectomized ducks involves an alpha-adrenergic mechanism.

Changes in plasma norepinephrine after intravertebral artery infusion of saralasin in sodium depleted dogs.

This study was designed to investigate the central action of circulating angiotensin II on the regulation of blood pressure in sodium depleted states. The effects of intravertebral arterial infusion of angiotensin II and [Sar-1, Ala-8] angiotensin II (saralasin) on plasma norepinephrine (NE) were studied in alpha-chloralose anesthetized dogs. Intravertebral arterial infusion of angiotensin II (10 ng/kg/min) increased mean arterial pressure (MAP), heart rate (HR) and plasma NE. Plasma NE was decreased by intravertebral arterial infusion of saralasin (0.40 +/- 0.05 to 0.28 +/- 0.04 ng/ml, p less than 0.05) in normal dogs. The administration of furosemide produced significant increases in plasma NE (142.4 +/- 23.7%, p less than 0.01), plasma renin activity (PRA) (158.6 +/- 26.3%, p less than 0.01) and HR (32.3 +/- 6.0 beats/min, p less than 0.01). A slight rise in mean blood pressure (3.9 +/- 1.2 mmHg, p less than 0.05) was observed during the furosemide administration. Saralasin infused into the vertebral artery significantly suppressed the furosemide-induced increases in plasma NE, HR and PRA, and lowered mean arterial blood pressure. Intravenous infusion of the same dose of saralasin produced no changes in arterial blood pressure, HR and plasma NE. These results suggest that the central sympathetic potentiation induced by circulating angiotensin II may contribute to the regulation of blood pressure in sodium and volume depleted states produced by furosemide.

Baroreflex sensitivity modulates vasodepressor response to nitroprusside.

Baroreflex activity is a determinant of the homeostatic response to alteration in blood pressure. We examined the factors that determine the magnitude of the vasodepressor response to sequential incremental intravenous infusions of sodium nitroprusside (NP), 0.05 to 6.4 micrograms/kg/min, in eight male patients with essential hypertension. Each infusion level was of 10 minutes' duration. Change from control values of mean arterial pressure (delta MAP), heart rate (delta HR) and plasma norepinephrine (delta NE) were obtained at the end of each infusion level. Significant correlations were found between delta MAP vs log dose NP, delta HR vs delta MAP and delta NE vs delta MAP for each patient (p less than 0.05). However, the slopes of these relationships varied widely between subjects and were significantly correlated with the control blood pressure of each patient. In addition, the sympathetic responsiveness, as measured by delta NE vs delta MAP, was inversely correlated with the degree of vasodepressor response seen. Thus, the magnitude of the vasodepressor response was determined by two major factors: 1) the predrug blood pressure, possibly reflecting altered vascular geometry with hypertension; 2) the degree of sympathetic response, which probably acts by mediating the degree of reflex alpha-adrenergic-mediated arteriolar vasoconstriction.

Hemodynamic and Catecholamine Changes after Administration of Naloxone

The hemodynamic and catecholamine response to intravenously administered naloxone, 0.2 mg and 0.4 mg, were determined in one group of surgical patients and one group of volunteers. Naloxone, 0.2 mg, was administered 30 minutes before the 0.4-mg dose. Group I consisted of six normotensive (IA) (aged 18 to 64, mean 35.7 years) and six hypertensive surgical patients (IB) (aged 35 to 67, mean 49.1 years) who were receiving a nitrous oxide, oxygen, and halothane anesthetic. Group II consisted of six normotensive (IIA) (aged 27 to 38, mean 36.1 years) and five hypertensive (IIB) unanesthetized volunteers (aged 41 to 60, mean 51.4 years). Mean arterial pressure, heart rate, plasma norepinephrine, epinephrine, and dopamine levels were compared before and after intravenous naloxone. Changes in mean arterial pressure, heart rate, plasma norepinephrine, epinephrine, and dopamine levels were not statistically significant in any group. This study suggests that intravenous naloxone, per se, alters neither mean arterial pressure, heart rate, or plasma catecholamine levels in normotensive or hypertensive humans.

Changes of Plasma and Cerebrospinal Fluid Noradrenaline during Frusemide Administration and Acute Renal Artery Constriction in Dogs

1. The effects of circulating angiotensin II on cerebrospinal fluid and plasma noradrenaline during frusemide administration and acute renal artery constriction were studied in dogs. 2. The administration of frusemide produced significant increases in cerebrospinal fluid and plasma noradrenaline. Intravertebral artery infusion of [Sar1, Ala8]angiotensin II (saralasin) significantly suppressed the frusemide-induced increases in cerebrospinal and plasma noradrenaline and resulted in a fall in arterial blood pressure. 3. Acute renal artery constriction produced the marked elevation of plasma noradrenaline and arterial blood pressure, although no significant increase was found in cerebrospinal fluid noradrenaline. Though intravertebral artery infusion of saralasin did not affect cerebrospinal fluid and plasma noradrenaline, intravenous infusion of saralasin reduced the increases in arterial blood pressure and plasma noradrenaline induced by acute renal artery constriction. 4. Plasma volume was significantly reduced by frusemide administration, but unchanged by acute renal artery constriction. 5. Therefore it is suggested that circulating angiotensin II may contribute to the regulation of blood pressure at least partially by acting on the central nervous system in the sodium- and volume-depleted states. However, the renin-angiotensin system appears to play a rather direct role in the mechanism of hypertension induced by renal artery constriction, not through the action of angiotensin II on the central sympathetic nervous system.

Release and clearance rates of epinephrine in man: importance of arterial measurements.

Previous estimates of catecholamine kinetics in human subjects have been based on the measurement of the catecholamine levels in forearm venous plasma. However, the use of forearm venous measurements may introduce considerable error, since venous catecholamine levels may primarily reflect metabolism in the organ drained rather than in the total body. In this study, arterial levels of epinephrine were found to significantly exceed forearm venous levels, both basally (mean +/- SEM, 71 +/- 13 vs. 50 +/- 7 pg/ml; n = 6; P less than 0.05) and during infusions of epinephrine [0.1 microgram/min (112 +/- 9 vs. 77 +/- 11 pg/ml; P less than 0.005) or 2 micrograms/min (862 +/- 71 vs. 437 +/- 66 pg/ml; P less than 0.001)]. During the 2 micrograms/min epinephrine infusion, arterial plasma norepinephrine rose from 191 +/- 37 to 386 +/- 78 pg/ml (P less than 0.001), while venous norepinephrine levels did not change significantly. Fractional extraction (arterial - venous + arterial X 100) of epinephrine across the forearm was 26 +/- 8% in the basal state and increased to 33 +/- 6% and further to 51 +/- 4% during the epinephrine infusions. The addition of propranolol (5 mg, iv, plus an 80 micrograms/min infusion) reduced fractional extraction from 51 +/- 4% to 35 +/- 5%. Whole body clearance of epinephrine, calculated from arterial measurements, was 33 +/- 3 ml/kg . min during the 0.1 microgram/min infusion and 35 +/- 3 ml/kg . min during the 2 micrograms/min epinephrine infusion, values 50% lower than the clearance rates calculated from venous measurements. Propranolol infusion resulted in a fall in whole body clearance to 20 +/- 2 ml/kg . min (P less than 0.001), suggesting that epinephrine clearance is partly dependent on a beta-adrenergic mechanism. Basal endogenous release rate (clearance X basal epinephrine level) was estimated to be approximately 0.18 microgram/min, a value much less than that reported in studies using venous measurements. We conclude that arterial rather than venous measurements should be used to estimate catecholamine kinetics in vivo.

Hemodynamic and Catecholamine Changes after Administration of Naloxone

The hemodynamic and catecholamine response to intravenously administered naloxone, 0.2 mg and 0.4 mg, were determined in one group of surgical patients and one group of volunteers. Naloxone, 0.2 mg, was administered 30 minutes before the 0.4-mg dose. Group I consisted of six normotensive (IA) (aged 18 to 64, mean 35.7 years) and six hypertensive surgical patients (IB) (aged 35 to 67, mean 49.1 years) who were receiving a nitrous oxide, oxygen, and halothane anesthetic. Group II consisted of six normotensive (IIA) (aged 27 to 38, mean 36.1 years) and five hypertensive (IIB) unanesthetized volunteers (aged 41 to 60, mean 51.4 years). Mean arterial pressure, heart rate, plasma norepinephrine, epinephrine, and dopamine levels were compared before and after intravenous naloxone. Changes in mean arterial pressure, heart rate, plasma norepinephrine, epinephrine, and dopamine levels were not statistically significant in any group. This study suggests that intravenous naloxone, per se, alters neither mean arterial pressure, heart rate, or plasma catecholamine levels in normotensive or hypertensive humans.

The role of presynaptic alpha-adrenoceptors in the regulation of blood pressure in the conscious rabbit.

1 Changes in mean arterial pressure, heart rate and plasma noradrenaline after alpha-adrenoceptor blockade with several alpha-adrenoceptor antagonists have been studied in the conscious rabbit in order to investigate the possible role of presynaptic alpha-adrenoceptors in cardiovascular regulation. 2 Prazosin (0.05-2 mg/kg) and phentolamine (0.5-20 mg/kg) produced dose-dependent falls in mean arterial pressure and rises in plasma noradrenaline. These changes were related to the degree of postsynaptic alpha-adrenoceptor blockade determined by the pressor response to intravenous phenylephrine. 3 Similar changes in mean arterial pressure and plasma noradrenaline were observed after administration of the direct vasodilators hydralazine (1-10 mg/kg) and nitroprusside (2.5-55 microgram kg-1 min-1). 4 After baroreceptor deafferentation by sinoaortic denervation the falls in mean arterial pressure were much greater and the rise in plasma noradrenaline was markedly attenuated. 5 Yohimbine (1 mg/kg) increased mean arterial pressure and plasma noradrenaline but it was not possible to exclude the possibility that central nervous effects of yohimbine underlay the increased sympathetic activity. 6 The magnitude of the baroreflex response to changes in pressure make it unlikely that the functional significance of the presynaptic alpha-adrenoceptor can be readily determined by measurement of plasma noradrenaline in intact animals.

Diet induced changes in sympatho-adrenal activity during submaximal exercise in relation to substrate utilization in man.

In order to study how the diet may influence sympatho-adrenal activity during exercise, 7 subjects were examined at rest and during submaximal exercise (25 min at 65% of VO2 max) on two occasions. The first occasion was preceded by 5 days on a carbohydrate poor diet (5% carbohydrate, 72% fat and 23% protein) and the second one by 5 days on a carbohydrate rich diet (78% carbohydrate, 8% fat and 14% protein) with the same energy content. Oxygen uptake, respiratory exchange ratio (R), heart rate and arterial plasma concentrations of adrenaline, noradrenaline, dopamine, insulin, glucose, lactate, free fatty acids (FFA), glycerol and beta-hydroxybutyrate were measured at rest and during exercise. Oxygen uptake and heart rate during exercise were higher and R was lower after the carbohydrate poor than after the carbohydrate rich diet. During exercise the arterial plasma concentrations of FFA, glycerol and beta-hydroxybutyrate were higher after the carbohydrate poor than after the carbohydrate rich diet whereas concentrations of insulin and lactate were lower. At rest arterial plasma noradrenaline and adrenaline levels were similar on the two diets (0.70 +/- 0.31 nM noradrenaline and 0.35 +/- 0.32 nM adrenaline one the carbohydrate rich diet, mean values +/- SD). Exercise induced increases in noradrenaline were more pronounced after the carbohydrate poor than after the carbohydrate rich diet (12.42 +/- 3.41 vs. 7.45 +/- 2.68 at 25 min of exercise, p less than 0.001). A similar, although more variable accentuation of exercise induced increases in adrenaline was found. It is concluded that, when compared to a carbohydrate rich diet, a carbohydrate poor diet increases the relative contribution of fat to oxidative metabolism and increases the sympatho-adrenal response to exercise. Stimulation of lipolysis by sympatho-adrenal mechanisms might be of importance for the substrate availability when carbohydrate intake in low.

Renal handling of dopa, dopamine, norepinephrine, and epinephrine in the dog.

The uptake and excretion of endogenous dopa, dopamine, norepinephrine, and epinephrine by the kidney were studied. Blood samples were taken from the aorta at the origin of the renal artery and from the renal vein during a timed urine collection in each of six anesthetised greyhound dogs. Arterial plasma dopa (1,043 +/- 129 pg/ml) and epinephrine (218 +/- 96 pg/ml) were consistently higher than venous levels of dopa (591 +/- 80) and epinephrine (54 +/- 16 pg/ml), showing extraction of these by the kidney, whereas arterial plasma norepinephrine (329 +/- 89 pg/ml) and dopamine (64 +/- 9 pg/ml) were lower than the venous levels of norepinephrine (695 +/- 161 pg/ml) and dopamine (239 +/- 45 pg/ml), indicating secretion of these catecholamines into the circulation. The dopa extracted did not appear in the urine. Norepinephrine (7.2 +/- 1.7 ng/min), epinephrine (4.5 +/- 1.7 ng/min), and dopamine (3.2 +/- 0.7 ng/min) were excreted in the urine. These rates of urinary excretion could be accounted for by glomerular filtration and tubular secretion of the three catecholamines. The kidney extracts circulating dopa. It extracts and excretes epinephrine, norepinephrine, and dopamine, and, in addition, secretes both dopamine and norepinephrine into the circulation. These observations emphasize the important relationship between renal function and the peripheral sympathetic nervous system.

Metabolic and hormonal adjustments during hemorrhage in cats after interference with the sympatho-adrenal system.

The relative contribution of the splanchnic sympathetic innervation and the adrenal medulla for metabolism and hormone secretion during two different levels of hemorrhagic hypotension was investigated in 3 groups of anesthetized cats, viz, intact, adrenalectomized and splanchnicotomized (adrenalectomy + cutting of splanchnic nerves). In intact cats, hemorrhage caused very marked elevations of arterial plasma glucose, adrenaline, noradrenaline, dopamine, lactate, cAMP, glycerol and glucagon concentrations whereas plasma insulin fell to only 20% of control values. Adrenalectomy attenuated the glucose, adrenaline, noradrenaline and cAMP responses whereas the normal insulin inhibition was abolished. Splanchnicotomy further reduced the hemorrhagic glucose and glycerol responses and, possibly, also that of glucagon. It is concluded that the adrenergic system as a whole is important for the adjustments of the release of glucose, cAMP, glycerol, insulin and glucagon that occur during hemorrhage in cats. The adrenal medulla seems to be of particular importance for the regulation of cAMP release.

Early effects of mild hypertension on the heart. A longitudinal study.

HomeHypertensionVol. 3, No. 6_pt_2Early effects of mild hypertension on the heart. A longitudinal study. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBEarly effects of mild hypertension on the heart. A longitudinal study. A G Logan, B W Gilbert, R B Haynes, B J Milne and P T Flanagan A G LoganA G Logan Search for more papers by this author , B W GilbertB W Gilbert Search for more papers by this author , R B HaynesR B Haynes Search for more papers by this author , B J MilneB J Milne Search for more papers by this author and P T FlanaganP T Flanagan Search for more papers by this author Originally published1 Nov 1981https://doi.org/10.1161/01.HYP.3.6_Pt_2.II-187Hypertension. 1981;3 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Cleophas T, Niemeyer M, Bernink P, Zwinderman K, Wijk A and Wall E (1996) Sequential comparison of therapy with beta-blockers and calcium channel blockers with celiprolol therapy in patients with angina pectoris, hypertension, or both, Current Therapeutic Research, 10.1016/S0011-393X(96)80012-9, 57:8, (614-621), Online publication date: 1-Aug-1996. Devereux R, Liebson P and Horan M (1987) Recommendations concerning use of echocardiography in hypertension and general population research., Hypertension, 9:2_pt_2, (II97), Online publication date: 1-Feb-1987.Liebson P, Devereux R and Horan M (1987) Hypertension research. Echocardiography in the measurement of left ventricular wall mass., Hypertension, 9:2_pt_2, (II2), Online publication date: 1-Feb-1987.Corea L, Bentivoglio M and Verdecchia P (1983) Echocardiographic left ventricular hypertrophy as related to arterial pressure and plasma norepinephrine concentration in arterial hypertension. Reversal by atenolol treatment., Hypertension, 5:6, (837-843), Online publication date: 1-Nov-1983. Messerli F (1983) Clinical determinants and consequences of left ventricular hypertrophy, The American Journal of Medicine, 10.1016/0002-9343(83)90118-3, 75:3, (51-56), Online publication date: 1-Sep-1983. November 1981Vol 3, Issue 6_pt_2 Advertisement Article InformationMetrics Copyright © 1981 by American Heart Associationhttps://doi.org/10.1161/01.HYP.3.6_Pt_2.II-187 Originally publishedNovember 1, 1981 PDF download Advertisement