New system for recording ambulatory blood pressure in man

Millar-Craig, M W; Hawes, Debra; Whittington, J. R.

doi:10.1007/bf02442453

Cited by 131 publications

(37 citation statements)

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“…The brachial artery in the nondominant arm was cannulated for continuous recording of intra-arterial pressure by the Oxford method. 25 Posture was carefully regulated throughout day 4 studies. Blood samples were obtained at 9:30 AM and 3:30 PM (as on day 1 of dosing) and at 9 PM.…”

Section: Acute and Chronic Endopeptidase Inhibitionmentioning

confidence: 99%

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Plasma brain natriuretic peptide and endopeptidase 24.11 inhibition in hypertension.

et al. 1993

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In contrast to the wealth of information available concerning the response of plasma atrial natriuretic peptide to changes in pressure and volume status and to inhibition of endopeptidase 24.11, very little is known of possible concomitant effects on brain natriuretic peptide. The effects of change in posture, pressor infusions of angJotensin II, or inhibition of endopeptidase 24.11 were documented in two groups of patients with essential hypertension receiving one of two orally active inhibitors (SCH 42495 or UK 79300) in double-blind, placebo-controlled, random-order crossover studies. Sustained (4 days) inhibition of endopeptidase 24.11 with either inhibitor significantly enhanced plasma atrial natriuretic peptide (/*<.O5, both groups) but suppressed plasma brain natriuretic peptide (P<.01, both groups) in association with significant falls in arterial pressure (/*<.O5, both groups). Assumption of the recumbent posture increased plasma atrial natriuretic peptide (20±5 vs 13±3 pmol/L, P<.05), whereas brain natriuretic peptide was unchanged (7±0J vs 7±0.4 pmol/L, NS). Pressor infusions of angiotensin II increased plasma levels of both atrial natriuretic peptide and brain natriuretic peptide (33 ±11 vs 17 ±4 pmol/L, P<.05, and 7.5±0.6 vs 5.5±0.4 pmol/L, / > <.O5, respectively). In contrast to atrial natriuretic peptide, brain natriuretic peptide probably is primarily regulated by left ventricular load rather than by atrial distending pressure. Thus, stimuli that incorporate substantial changes in arterial pressure may induce acute and chronic concordant changes in plasma brain natriuretic peptide, whereas other events that alter central blood volume and atrial stretch without major concomitant changes in arterial pressure will alter plasma atrial natriuretic peptide but not brain natriuretic peptide. (Hypertension 1993,22:231-236) KEY WORDS • natriuretic peptides, brain • hypertension, essential blood pressure • posture • membrane metalloendopeptidase natriuretic peptides, atrial • B rain natriuretic peptide (BNP) is the second member of the family of natriuretic peptides to be discovered and characterized. 1 Originally detected in porcine brain, it is present in greatest concentrations in cardiac tissue. 24 Although small amounts of BNP may be cosecreted with atrial natriuretic peptide (ANP) from specific atrial myocyte granules, 5 the predominant source of circulating BNP appears to be through constitutive secretion from ventricular myocytes. 6 In healthy individuals, circulating plasma concentrations of BNP are lower than concurrent levels of ANP. However, in patients with cardiac impairment levels rise to equal or exceed plasma ANP, and, similar to ANP, increments in BNP are related to the severity of cardiac disease. 67 It remains unclear whether hypertension is associated with any significant consistent disturbance in plasma BNP, but at least some reports indicate BNP is increased in proportion to left ventricular hypertrophy (LVH), left ventricular load, or both.8 BNP and ANP exhibit a similar array o...

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Section: Acute and Chronic Endopeptidase Inhibitionmentioning

confidence: 99%

“…Subjects remained recumbent overnight (9 PM to 8 AM) (with blood samples taken at 10 PM, 1 AM, and 8 AM) and were then seated for an hour before a sample was taken at 9 AM on day 5 of dosing. Intra-arterial pressure recordings 25 were performed through the inpatient study periods.…”

Section: Posturementioning

confidence: 99%

Plasma brain natriuretic peptide and endopeptidase 24.11 inhibition in hypertension.

et al. 1993

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“…The nondominant brachial artery was cannulated for measurement of blood pressure by the Oxford continuous recording technique. 8 Subjects were seated throughout the studies except for standing to pass urine every 30 minutes. Urinary indexes measured included volume, sodium, potassium, calcium, magnesium, phosphate, creatinine, and cyclic guanosine monophosphate (cGMP).…”

Section: Atrial Natriuretic Factor In Hypertensionmentioning

confidence: 99%

Atrial natriuretic factor in hypertension: bioactivity at normal plasma levels.

et al. 1989

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To ascertain whether small shifts in plasma atrial natriuretic factor (ANF) exerted biological effects in hypertension, we studied the renal, hemodynamic, and hormonal effects of ANF ] infused at a dose (0.75 pmol/kg/min for 3 hours) that would induce changes in plasma ANF confined to the normal, resting range, in a group of six young men with uncomplicated, mild essential hypertension. During ANF infusions, the patients excreted 11.8±2.0 mmol (mean±SEM) sodium more than during the time-matched placebo phase natriuresis (/><0.001, mean increase of 53% above placebo values). Urinary excretion of cyclic guanosine monophosphate rose to more than double (212%, p< 0.001) placebo values. Plasma renin activity (0.4±0.05 vs. 0.9±0.12 nmol/l/hr, /?<0.0001) and aldosterone concentrations (102±4 vs. 184±47 pmol/l, p<0.05) were clearly suppressed during administration of ANF. Plasma norepinephrine also fell significantly below placebo values (268±17 vs. 439±35 pg/ml, p<0.05). Urine volume, the excretion of electrolytes other than sodium, hematocrit, effective renal plasma flow, glomerular filtration rate, and filtration fraction were unaffected by ANF. Similarly, plasma concentrations of epinephrine, arginine vasopressin, adrenocorticotropic hormone, and cortisol were unchanged. Blood pressure and heart rate were unchanged. Minor perturbations in plasma ANF concentrations exert clear biological effects in patients with mild essential hypertension. These data suggest that such minor shifts in plasma ANF are of physiological relevance in mild hypertension and probably contribute to volume homeostasis in this condition. {Hypertension 1989;14:261-268) A trial natriuretic factor (ANF) continues to / \ attract intense interest as a potentially major .Z \ . regulator of body fluid volumes and arterial pressure. Studies in humans have clearly demonstrated that this peptide may induce natriuresis, suppress the renin-angiotensin-aldosterone system, and lower arterial pressure.1 -3 Recently, we demonstrated that such effects occur in normotensive subjects even with low doses of ANF, which induce perturbations in plasma peptide concentrations entirely within the resting normal range. 4 Far less is known concerning the effect of physiological doses of ANF in hypertensive patients. The response to high doses of ANF appears qualitatively similar in both normotensive and hypertensive subjects. 5 -6 However, data suggest the natriuretic effect of ANF is partially pressure dependent and thus is enhanced in hypertension.

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“…The technique of ambulatory blood pressure monitoring used in this laboratory has been fully documented previously (Millar-Craig et al, 1978b). Briefly, a French 3 gauge cannula (Seldicath) was introduced into the brachial artery of the non-dominant arm, under local anaesthesia.…”

Section: Intra-arterial Ambulatory Blood Pressure Recordingmentioning

confidence: 99%

24 h blood pressure control with the once daily calcium antagonist, amlodipine.

Heber

Brigden

Al-Khawaja

et al. 1989

Brit J Clinical Pharma

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1 Amlodipine is a novel calcium antagonist which, although pharmacologically similar to other dihydropyridine calcium antagonists, has a long plasma half-life, permitting steady state blood levels to be achieved with a once-daily dose regimen. 2 We have performed a study to examine the effects of this drug on the blood pressure of hypertensive patients over a 24 h period. After a placebo run-in, the drug was administered to 11 patients at a starting dose of 5 mg, and increased to 10 mg after 2 weeks of treatment if the cuff diastolic blood pressure response was unsatisfactory. Cuff measurements were made at entry, after 2 weeks treatment with placebo, after 2 weeks on amlodipine 5 mg once daily, and after a further 4 weeks on amlodipine 5 mg or 10 mg once daily. Intraarterial blood pressure recordings were made at the end of the placebo phase and at completion of the study. 3 Mean supine blood pressure measured sphygmomanometrically was 168/103 (n = 11) mm Hg at entry, 169/104 (n = 11) mm Hg at the end of the placebo phase, 153/95 (n = 11) mm Hg after 2 weeks of treatment and 146/92 (n = 11) mm Hg at the end of the study. Blood pressure curves plotted for each phase of the study revealed an effective 24 h duration of action. Mean daytime blood pressure was reduced from 165/103 to 147/89 mm Hg (P < 0.05, n = 10), and mean night-time blood pressure was reduced from 137/79 to 121/69 mm Hg (P < 0.05, n = 10). There was no change in heart rate. 4 One patient developed ankle swelling which would have required discontinuation of medication had she not already been at the end of the study. The drug was otherwise well tolerated. 5 These results indicate that amlodipine is effective as a once daily antihypertensive agent, and is well tolerated.

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New system for recording ambulatory blood pressure in man

Cited by 131 publications

References 0 publications

Plasma brain natriuretic peptide and endopeptidase 24.11 inhibition in hypertension.

Plasma brain natriuretic peptide and endopeptidase 24.11 inhibition in hypertension.

Atrial natriuretic factor in hypertension: bioactivity at normal plasma levels.

24 h blood pressure control with the once daily calcium antagonist, amlodipine.

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