Differential Blood Pressure and Hormonal Effects after Glucose and Xylose Ingestion in Chronic Autonomic Failure

1989 ◽  
Vol 77 (1) ◽  
pp. 85-92 ◽  
Author(s):  
C. J. Mathias ◽  
D. F. da Costa ◽  
C. M. McIntosh ◽  
P. Fosbraey ◽  
R. Bannister ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Area Under Curve ◽  
Autonomic Failure ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Oral Glucose ◽  
Postprandial Hypotension ◽  
Hormonal Effects

1. To investigate whether carbohydrate contributes to postprandial hypotension in autonomic failure, the cardiovascular, biochemical and hormonal effects of oral glucose and an iso-osmotic solution of oral xylose were studied on separate occasions in six patients with chronic autonomic failure. The effects of oral glucose were also studied in eight normal subjects. 2. In the patients oral glucose lowered blood pressure substantially (−34 ± 7% at 60 min, area under curve −24.9 ± 3.5%, P < 0.001) and for a prolonged period (− 25 ± 4% at 120 min). Plasma noradrenaline levels did not change. In the normal subjects blood pressure was unchanged and plasma noradrenaline rose, suggesting a compensatory increase in sympathetic nervous activity. 3. In the patients xylose caused a smaller and more transient fall in blood pressure (−15 ± 6% at 90 min, area under curve −8.9 ± 4%, P < 0.05) with a non-significant elevation in packed cell volume (36.7 ± 1.8 to 38.2 ± 1.8). It was therefore unclear if xylose was exerting osmotic effects within the bowel which contributed to the small blood pressure fall. Packed cell volume did not change in either the patients or normal subjects after glucose. 4. In the patients and normal subjects plasma insulin rose after glucose. Insulin levels were unchanged after xylose. Levels of pancreatic polypeptide and neurotensin, a potential vasodilator, rose in the patients only. The latter rose to a similar extent after both glucose and xylose, making it unlikely that neurotensin alone accounted for the hypotension. 5. These studies indicate that the carbohydrate components of a meal, and in particular those causing insulin release, contribute to postprandial hypotension in patients with autonomic failure.

Effects of hyperinsulinaemia on the cardiovascular responses to graded hypovolaemia in normal and diabetic subjects

1988 ◽  
Vol 75 (1) ◽  
pp. 85-92 ◽  
Author(s):  
A. R. Scott ◽  
T. Bennett ◽  
I. A. MacDonald
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Normal Male ◽  
Euglycaemic Clamp ◽  
Arterial Blood ◽  
Hyperinsulinaemic Euglycaemic Clamp

1. Two experiments were carried out. The first with five normal male subjects was placebo controlled and single blind, each subject being studied on two occasions. Lower body subatmospheric pressure (LBSP) was used to assess the cardiovascular effects of graded hypovolaemia before and during either a hyperinsulinaemic, euglycaemic clamp or a placebo clamp using 0.9% (w/v) NaCl only. 2. During hyperinsulinaemia, resting systolic blood pressure rose and was accompanied by forearm vasodilatation. Forearm blood flow (FABF) and heart rate (HR) were higher at each level of LBSP during than before hyperinsulinaemia. In addition, hyperinsulinaemia was accompanied by a small increase in noradrenaline, but packed cell volume did not change. 3. In the second experiment, the effects of a hyperinsulinaemic euglycaemic clamp on the cardiovascular responses to LBSP were assessed in seven diabetic subjects with peripheral and autonomic neuropathy. 4. In contrast to the normal subjects, there was a slight fall in systolic blood pressure during the clamp but no effect was noted on HR or FABF. Mean arterial blood pressure was lower at each level of LBSP during hyperinsulinaemia compared with the pre-elamp period. Packed cell volume fell during the clamp and plasma noradrenaline rose. In one of the diabetic subjects, a precipitous fall in blood pressure occurred during hyperinsulinaemia when LBSP of 10 mmHg (1.3 kPa) was applied, this manoeuvre having been well tolerated before the clamp. 5. The mode of action of hyperinsulinaemia is not clear, but there was, however, no evidence that a fall in plasma volume had occurred.

Pressor effect of arginine vasopressin in progressive autonomic failure

1986 ◽  
Vol 71 (2) ◽  
pp. 173-178 ◽  
Author(s):  
T. D. M. Williams ◽  
D. DaCosta ◽  
C. J. Mathias ◽  
R. Bannister ◽  
S. L. Lightman
Keyword(s):  
Blood Pressure ◽  
Arginine Vasopressin ◽  
Autonomic Failure ◽  
Pressor Response ◽  
Normal Subjects ◽  
Pressor Effect ◽  
Normal Volunteers ◽  
Pressor Responses ◽  
Transient Bradycardia ◽  
Related Increase

1. The blood pressure (BP) and heart rate (HR) responses to 5 min incremental intravenous infusions of noradrenaline (NA) and arginine vasopressin (AVP) were investigated both in patients with progressive autonomic failure (PAF) and in normal volunteers. 2. Stepwise infusion of NA at rates of 300–3000 pmol min−1 kg−1 produced a bradycardia and a dose related increase in BP in normal subjects. In subjects with PAF there was no significant HR response but the dose-BP response was shifted to the left with significant pressor responses at infusion rates of 60–300 pmol min−1 kg−1. 3. Stepwise infusion of AVP at 0.2–5.0 pmol min−1 kg−1 caused transient bradycardia but no pressor response in seven normal volunteers. Further increases in AVP infusion in three other subjects achieved plasma AVP levels as high as 3000–4000 pmol/l, and still no significant pressor response was observed. 4. Stepwise infusion of AVP at 0.05–2.0 pmol min−1 kg−1 in the eight subjects with PAF resulted in a pressor response without any change in HR. During this infusion plasma AVP increased from 0.8 ± 0.2 (mean ± se) to 30 ± 2 pmol/l. A significant pressor response was already apparent at a plasma AVP level of 5.5 ± 1.8 pmol/l.

Oestradiol-induced hypotension in spontaneously hypertensive rats: putative role for intracellular cations, sodium-potassium flux and prostanoids

1992 ◽  
Vol 82 (4) ◽  
pp. 389-395 ◽  
Author(s):  
C. Stonier ◽  
J. Bennett ◽  
E. A. Messenger ◽  
G. M. Aber
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Spontaneously Hypertensive

1. The effect of oestradiol alone and in combination with indomethacin on blood pressure, erythrocyte cation concentration and Na+−K+ flux has been studied in adult female normotensive and spontaneously hypertensive rats. 2. Oestradiol alone resulted in a significant decrease in blood pressure in spontaneously hypertensive rats (from 165.3 ± 3.9 to 146.4 ± 2.7 mmHg, P < 0.001), whereas it induced a significant increase in normotensive rats (from 111.8 ± 1.8 to 124.1 ± 3.6 mmHg, P < 0.001). When indomethacin and oestradiol were administered simultaneously or when indomethacin was given alone, no change in blood pressure occurred in spontaneously hypertensive rats (158.6 ± 6.9 and 159.8 ± 6.2 mmHg, respectively). 3. The fall in blood pressure induced by oestradiol in spontaneously hypertensive rats was associated with significant reductions in erythrocyte K+ concentration (from 127.4 ± 1.2 to 116.9 ± 1.7 mmol/l of cells, P < 0.001), in erythrocyte Na+ concentration (from 14.3 ± 0.8 to 13.0 ± 0.6 mmol/l of cells, P < 0.02), in ouabain-sensitive erythrocyte Na+ flux (from 17.8 ± 0.3 to 16.0 ± 0.4 mmol h−1 (1 of cells)−1, P < 0.01) and in ouabain-sensitive erythrocyte K+ flux (from 11.4 ± 0.2 to 10.4 ± 0.2 mmol h−1 (1 of cells)−1, P < 0.01). No change in blood pressure, erythrocyte cation concentration or Na+−K+ flux occurred when oestradiol and indomethacin were given together or when indomethacin was administered alone. 4. The hypertensive influence of oestradiol in normotensive rats was unaccompanied by any changes in erythrocyte K+ concentration, erythrocyte Na+ concentration and total, ouabain-sensitive and ouabain-resistant Na+−K+ flux. 5. The divergent changes in blood pressure noted in the two strains occurred despite comparable changes in plasma renin activity after oestradiol, with significant increases in plasma renin activity in normotensive rats (from 16.4 ± 4.2 to 28.4 ± 6.6 ng of angiotensin I h−1 ml−1, P < 0.05) and in spontaneously hypertensive rats (from 28.3 ± 2.7 to 39.5 ± 5.7 ng of angiotensin I h−1 ml−1, P < 0.01). The plasma renin activity in spontaneously hypertensive rats receiving oestradiol or indomethacin and oestradiol were similar with values of 39.5 ± 5.7 and 40.6 ± 5.7 ng of angiotensin I h−1 ml−1, respectively, but were significantly higher than that seen in control animals (28.3 ± 2.7 ng of angiotensin I h−1 ml−1, P < 0.01). Similarly, indomethacin alone induced a significant increase in plasma renin activity in spontaneously hypertensive rats to 35.8 ± 7.6 ng of angiotensin I h−1 ml−1 (P < 0.05). 6. The contrasting effects of oestradiol on blood pressure in the two rat strains occurred without any change in packed cell volume. Likewise, the changes in blood pressure in spontaneously hypertensive rats with either oestradiol alone or in combination with indomethacin occurred without any change in packed cell volume, although indomethacin alone resulted in a significant reduction in packed cell volume (from 30.9 ± 1.6 to 26.8 ± 2.0, P < 0.01). 7. The results suggest that the hypotensive action of oestradiol in spontaneously hypertensive rats might be mediated through its influence on erythrocyte cation concentration and/or the modulation of Na+−K+ flux either directly or via the action of prostanoids.

Endogenous Opioids Modulate Central Nervous System Blood Pressure Control in Man

1982 ◽  
Vol 63 (s8) ◽  
pp. 331s-333s ◽  
Author(s):  
P. C. Rubin ◽  
Kathleen McLean ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Pressure Control ◽  
Normal Subjects ◽  
Pressure Control ◽  
Endogenous Opioids ◽  
Plasma Noradrenaline ◽  
Head Up Tilt ◽  
Blind Manner

1. Two studies were performed to elucidate the role of opioids in blood pressure control in man. 2. Study 1: nine normal subjects, 18–32 years, received in a randomized single blind manner, volume matched infusions of a Met-enkephalin analogue (DAMME) 0.5 mg, naloxone 0.2 mg/kg or saline. Blood pressure, heart rate and plasma noradrenaline were determined supine and after a 5 min, 70° head-up tilt at 0, 3/4, 2, 3, 4, 5 and 6 h. 3. Study 2: seven subjects, after baseline recordings of blood pressure and heart rate received six incremental infusions of sodium nitroprusside, 1.5–7.5 μg min−1 kg−1. They then received DAMME or naloxone and the nitroprusside infusions were repeated between 3 and 4 h. There was a significant linear relationship between fall in mean arterial pressure and rise in heart rate in each case and the slope was used as an index of baroreflex sensitivity. 4. Neither naloxone nor DAMME influenced supine blood pressure or heart rate. Blood pressure after head-up tilt was significantly (analysis of variance) decreased by DAMME for up to 5 h but not by naloxone, the effect being most marked at 3 h: systolic (mean ± sd), placebo 110 ± 6, naloxone 106 ± 10, DAMME 96 ± 16 (P< 0.02); diastolic (mean ± sd), placebo 78 ± 7, naloxone 79 ± 5, DAMME 67 ± 8 (P < 0.01). The increases in heart rate and plasma noradrenaline on tilting after DAMME were not significantly different from values with placebo or naloxone. The 3 h values for heart rate were: placebo 87 ± 16, naloxone 88 ± 19, DAMME 89 ± 23 (P > 0.1); for plasma noradrenaline (nmol/l): placebo 6.0 ± 2.2, naloxone 5.8 ± 1.9, DAMME 6.0 ± 1.9 (P > 0.1). 5. Naloxone significantly increased the slope (beats per min/mmHg) of the regression relationship from a mean of 1.8 ± 0.07 to 3.0 ± 1.3 (P < 0.05), and DAMME reduced the slope from 2.7 ± 1.7 to 1.2 ± 0.5 (P < 0.05). 6. We conclude that endogenous opioids modulate baroreflex function in man.

Effects of Meal Composition on the Postprandial Blood Pressure, Catecholamine and Insulin Changes in Elderly Subjects

1989 ◽  
Vol 77 (3) ◽  
pp. 265-272 ◽  
Author(s):  
J. F. Potter ◽  
D. Heseltine ◽  
G. Hartley ◽  
J. Matthews ◽  
I. A. Macdonald ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Plasma Insulin ◽  
Autonomic Function ◽  
High Protein ◽  
Elderly Subjects ◽  
High Fat ◽  
High Carbohydrate

1. The effects of four meals of similar energy, but different nutritional, composition on postprandial blood pressure, heart rate, autonomic function, catecholamines, insulin and packed cell volume levels were studied in seven fit elderly subjects. 2. The high carbohydrate and high protein meals led to a significant overall fall in supine systolic and diastolic blood pressure compared either with no change or a rise after the normal (i.e. mixed) and high fat meals. Similar between-meal differences were seen with erect diastolic but not erect systolic blood pressure. No significant postural blood pressure fall occurred after any of the meals. Supine heart rate was unaffected by meal type or by time, and although erect heart rate showed a small increase during the study there was no between-meal difference. 3. Parasympathetic function was unaffected by meal type. Plasma noradrenaline rose after the high carbohydrate and mixed meals only, remaining elevated for 120 min after meal consumption. This increase was not related to the changes in blood pressure or plasma insulin levels. 4. Plasma insulin and glucose rose after the high carbohydrate and mixed meals, but were unchanged after the high protein and high fat meals. Packed cell volume showed a small decrease towards the end of the study, although there was no between-meal variation. 5. The differences in the cardiovascular changes after the different meals could not be ascribed to alterations in autonomic function, insulin release or fall in plasma volume. We propose that the postprandial changes in blood pressure are due to the nutrient composition of the meal rather than the actual energy load.

Circulating Dopamine: Its Effect on the Plasma Concentrations of Catecholamines, Renin, Angiotensin, Aldosterone and Vasopressin in the Conscious Dog

1981 ◽  
Vol 61 (4) ◽  
pp. 417-422 ◽  
Author(s):  
S. G. Ball ◽  
M. Tree ◽  
J. J. Morton ◽  
G. C. Inglis ◽  
R. Fraser
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Control Period ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Dopamine Infusion ◽  
Renin Angiotensin ◽  
Arterial Blood

1. Six male beagle dogs with carotid loops were infused with sodium chloride solution (150 mmol/l: saline) during control observations followed by dopamine infusion at various rates. Arterial blood samples were drawn during the control period and at the end of each period of dopamine infusion for the measurement of plasma dopamine, noradrenaline, adrenaline, renin, angiotensin II, aldosterone, vasopressin, electrolytes and packed cell volume. Blood pressure and pulse were recorded throughout. 2. The rate of infusion and plasma dopamine levels were closely correlated (r = 0.99, P < 0.001). Plasma dopamine levels two to 20 times basal values produced no significant change in any of the other variables measured; levels 200 times basal values caused a significant increase (P < 0.05) in plasma renin concentration; levels 2000 times basal values were associated with significant increases (P < 0.05) in plasma renin and angiotensin II, packed cell volume and blood pressure, without significant changes in other measurements. 3. Circulating dopamine is unlikely to be important in the control of sodium and water metabolism.

Blood pressure control and erythrocytosis in rats: theory and observations

1994 ◽  
Vol 72 (6) ◽  
pp. 679-686 ◽  
Author(s):  
Anne B. Gould ◽  
Susan Goodman ◽  
Charles Swartz
Keyword(s):  
Blood Pressure ◽  
Cell Volume ◽  
Blood Volume ◽  
Packed Cell Volume ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Pressure Control ◽  
Peripheral Vascular ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

We compared some of our latest experiments on blood pressure control and erythrocytosis in spontaneously hypertensive rats with Gaar's computer-simulated studies, which suggest that erythrocytosis is a key to understanding the hemodynamic changes in hypertension. We tested two of Gaar's several predictions: (i) peripheral vascular resistance decreases when the feedback control of erythrocytosis is blocked and (ii) in primary hypertension, blood volume is increased slightly. We also studied the interrelation of systolic blood pressure and plasma renin substrate in spontaneously hypertensive rats, and the effect of diet on renin, blood pressure, and erythrocytosis. Our data showed that (i) on a percentage basis the renin system supports blood pressure essentially in the same manner in normal and hypertensive rats, (ii) peripheral vascular resistance decreased when erythrocytosis was partially blocked by feeding a low-iron diet, (iii) blood volume was similar in normal and hypertensive rats, and (iv) dextrin stimulates plasma renin, packed cell volume, and blood pressure in hypertensive rats. We conclude that blood pressure and erythrocytosis are interrelated, that the combined data of simulated and experimental studies support the notion that primary hypertension is a blood-vessel adaptation in response to a renal energy need that may require additional oxygen.Key words: angiotensinogen, renin, dextrin, packed cell volume.

Prolonged Decrease in Blood Pressure after Atrial Natriuretic Peptide Infusion in Essential Hypertension: A New Anti-Pressor Mechanism?

1989 ◽  
Vol 77 (3) ◽  
pp. 253-258 ◽  
Author(s):  
D. R. J. Singer ◽  
N. D. Markandu ◽  
M. G. Buckley ◽  
M. A. Miller ◽  
A. L. Sugden ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Cell Volume ◽  
Natriuretic Peptide ◽  
Packed Cell Volume ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
High Sodium

1. To study the anti-hypertensive effects of atrial natriuretic peptide (ANP), eight patients with mild to moderate essential hypertension, on no treatment, were infused with α-human ANP (102–126) (37 pmol min−1 kg−1) or placebo for 60 min and observed for a further 4 h on the fifth day of low and high sodium diets in a randomized, cross-over study. 2. Plasma ANP levels increased over 30-fold into the high pathophysiological range during ANP infusion, but had returned to control values by 60 min after the end of infusion. With ANP infusion, there was a large decrease in supine blood pressure which was similar on both the low and high sodium intakes and was maximal 20–40 min after completion of the infusion. These reductions in blood pressure were sustained for a further 4 h after the end of ANP infusion and for 3 h after plasma ANP levels had returned to control values. 3. Maximal urinary sodium excretion increased 10-fold on the low sodium diet (negative sodium balance 20 mmol) and threefold on the high sodium diet (negative sodium balance 30 mmol) during ANP infusion; however, during the 4 h after infusion, urinary sodium excretion was below placebo values. During ANP infusion, packed cell volume increased significantly on both diets but returned to control values by 4 h after the end of infusion. 4. There were no significant changes in plasma renin activity compared with placebo during or after ANP infusion. However, plasma aldosterone was significantly greater than placebo values after the end of ANP infusion on both low and high sodium diets. 5. The sustained fall in blood pressure after ANP infusion appears to be unexplained by changes in sodium balance, packed cell volume and plasma ANP levels. These findings suggest that ANP may have a prolonged action on a pressor mechanism which remains to be defined.

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