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(Hypertension. 2000;36:e3.)
© 2000 American Heart Association, Inc.

Hypertension Electronic Pages

Vasopressin and Blood Pressure in Humans

Jens Jordan; Jens Tank

Clinical Research Center, Franz Volhard Klinik, Charite, Humboldt University, Berlin, Germany

Andre Diedrich; David Robertson; John R. Shannon

Nathan Blaser Shy-Drager Research Program, Autonomic Dysfunction Center, Vanderbilt University, Nashville, Tennessee

	Introduction

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To the Editor:

The importance of vasopressin for blood pressure regulation in humans has been a matter of debate for the past few decades. In healthy subjects, pharmacological blockade of vascular vasopressin (VI) receptors leads to no or minimal changes in arterial blood pressure.¹ This observation suggests that in the presence of intact function of the autonomic nervous system and the renin-angiotensin-aldosterone system, vasopressin release may be of minor importance for the maintenance of blood pressure. However, with impaired autonomic nervous system function or renin-angiotensin-aldosterone system function, vasopressin release may serve as a back-up mechanism to prevent excessive hypotension. For example, the hypotension in vasovagal syncope and pure autonomic failure^{2 3} and during ganglionic blockade^{4 5} is associated with a substantial increase in plasma vasopressin concentration. In this study, we applied short hypotensive stimuli during ganglionic blockade to further elucidate the role of vasopressin in blood pressure regulation in humans.

We studied 10 healthy subjects (5 men, 5 women, 33±1.9 years). In all studies, the heart rate was determined by continuous electrocardiogram and the blood pressure was measured by a radial artery catheter. In an initial study, 7 subjects underwent a battery of cardiovascular autonomic reflex tests before and during complete blockade of autonomic ganglia with trimethaphan.⁵ Before ganglionic blockade, the respiratory sinus arrhythmia ratio was 1.4±0.09. Blood pressure increased 26±4/21±3.7 and 34±1.5/26±2.0 mm Hg with sustained handgrip and cold pressor testing, respectively. Blood pressure did not decrease from baseline during phase 2 of the Valsalva maneuver (40 mm Hg intrathoracic pressure for 15 seconds), but blood pressure increased 19±4.8/12±3.0 mm Hg above the baseline value during phase 4.

With ganglionic blockade, blood pressure decreased from 129±4.3/67±3.2 mm Hg to 94±4.5/52±2.2 mm Hg and the plasma norepinephrine concentration decreased from 190±27 pg/mL to 39±8.3 pg/mL (P<0.01). Plasma renin activity did not change despite the profound decrease in blood pressure. Plasma vasopressin concentration was 1.6±0.13 pg/mL at baseline and increased to 27±15 pg/mL during ganglionic blockade (P<0.01). Ganglionic blockade abolished the respiratory sinus arrhythmia and the pressor response to handgrip and cold pressor testing. Blood pressure decreased 39±7.7/20±5.1 mm Hg during phase 2 of the Valsalva maneuver, and the blood pressure overshoot during phase 4 was eliminated. In 4 subjects, we observed a pressor response that started 30 seconds after completion of the Valsalva maneuver. The pressor response reached a maximum of 21±5/15±6 mm Hg above baseline and was sustained for >3 minutes in all subjects.

In a subsequent study in 6 subjects, we tested the hypothesis that this delayed pressor response in the absence of autonomic nervous system function might be related to a release of catecholamines or vasopressin or to an increase in plasma renin activity. During trimethaphan infusion, which was at a stable rate for at least 60 minutes to allow for the stabilization of neurohumoral mechanisms, venous blood samples were obtained. Study subjects then performed the Valsalva maneuver for 15 seconds. Venous blood was again obtained 90 seconds after completion of the maneuver. Blood pressure decreased profoundly during phase 2, and the blood pressure overshoot during phase 4 was absent (Figure, top). Blood pressure increased from 98±3.5/55±1.8 mm Hg at baseline to a maximum of 114±5.1/66±4.6 mm Hg 125±20 seconds after the completion of the Valsalva maneuver (P<0.05). Plasma vasopressin concentration increased 3-fold, from 16±5.4 pg/mL before the Valsalva maneuver to 49±9.5 pg/mL 90 seconds after the Valsalva maneuver (P<0.05) (Figure, bottom). In contrast, plasma renin activity and plasma catecholamines did not change.

View larger version (17K): [in this window] [in a new window]   Figure 1. Figure. (top) Systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) before, during, and after a Valsalva maneuver that was conducted during complete ganglionic blockade. During phase II of the Valsalva maneuver (II), blood pressure decreased profoundly. The neurally mediated blood pressure overshoot during phase IV was absent. Baroreflex-mediated heart rate changes were abolished. After the Valsalva maneuver, blood pressure increased markedly. (bottom) Plasma vasopressin concentration before and after the Valsalva maneuver. After the Valsalva maneuver, plasma vasopressin concentration increased markedly in each subject.

We conclude that in some normal subjects, acute hypotension during ganglionic blockade is followed by a delayed and sustained pressor response. The temporal association of the delayed pressor response and vasopressin release suggests that vasopressin contributes to blood pressure control in humans in the setting of impaired autonomic nervous system function. Assessment of vasopressin release during ganglionic blockade provides a unique tool to characterize afferent and central parts of the baroreflex that are not accessible with conventional baroreflex tests.

Dr. Jordan is supported by the Deutsche Forschungsgemeinschaft.

	References

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1. Bussien JP, Waeber B, Nussberger J, Schaller MD, Gavras H, Hofbauer K, Brunner HR. Does vasopressin sustain blood pressure of normally hydrated healthy volunteers? Am J Physiol. 1984;246:HI43–HI47.
2. Kauftnann H, Oribe E, Miller M, Knott P, Wiltshire-Clement M, Yahr MD. Hypotension induced vasopressin release distinguishes between pure autonomic failure and multiple system atrophy with autonomic failure. Neurology. 1992;42:590–593.[Abstract/Free Full Text]
3. Zerbe RL, Henry DP, Robertson GL. Vasopressin response to orthostatic hypotension: etiologic and clinical implications. Am J Med. 1983;74:265–271.[Medline] [Order article via Infotrieve]
4. Baylis PH, Robertson GL. Osmotic and non-osmotic stimulation of vasopressin release [Proceedings]. J Endocrinol. 1979;83:39P–40P.
5. Jordan J, Shannon JR, Black BK, Lance RH, Squillante MD, Costa F, Robertson D. N_n-nicotinic blockade as an acute human model of autonomic failure. Hypertension. 1998;31;1178–1184

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