Effects of antihypertensive treatment on vasopressin secretion and on its osmoregulation in moderate hypertension

Alberto Del Bo, Sandra Suraci, Marianna Giuditta, Martina Mistò, Alberto Zanchetti

Research output: Contribution to journalArticle

Abstract

Background. Changes in plasma osmolality and arterial pressure can affect the secretion of vasopressin (AVP). Objective. To investigate the effect of a drug-induced lowering of the arterial pressure on the plasma concentration of AVP and on its osmoregulation in moderately severe uncomplicated hypertensives. Design and methods. A group of 33 moderate uncomplicated and untreated essential hypertensives of both sexes (mean age 48 ± 1 years, average arterial pressure 171 ± 3/108 ± 2 mmHg) was studied. We measured AVP and other plasma and urine variables in 21 of them before and after administration of a hypertonic NaCl solution (100 mmol NaCl in 50 ml). Antihypertensive treatment with a single drug or, if necessary, with a combination of drugs was initiated for eight of these subjects and hypertonic saline administration was repeated after 1 month of treatment. The hypertonic stimulus was administered to the other 12 subjects after acute lowering of the arterial pressure by continuous intravenous infusion either of 0.3 mg clonidine in 100 ml (n = 6) or of 50 mg sodium nitroprusside in 250 ml (n = 6). Results. Administration of hypertonic saline to untreated hypertensives increased their AVP level from 1.6 ± 0.28 to 5.4 ± 0.7 pg/ml (n = 21, P <0.01). Their mean arterial pressure was lowered after pharmacological treatment for 1 month (n = 8) from 125 ± 2 to 101 ± 2 mmHg; their baseline AVP level remained unchanged (1.2 ± 0.21 versus 0.9 ± 0.25 pg/ml); after hypertonic saline had been administered to hypertensives with lowered arterial pressures, their AVP level increased to 6.0 ± 1.03 pg/ml (P <0.01). The AVP level in subjects whose MAP had been lowered acutely by administration of clonidine (n = 6) or of sodium nitroprusside (n = 6; on the average, from 132 ± 3 to 110 ± 4 mmHg) increased concurrently from 1.6 ± 0.63 to 3.4 ± 0.7 pg/ml (P <0.05); after administration of the hypertonic saline the AVP level increased to 10.8 ± 2.22 pg/ml (P <0.01). This stimulated value was significantly (P <0.01) higher than that observed after hypertonic saline had been administered to untreated hypertensives (5.4 ± 0.7 pg/ml). Conclusions. Acute lowering of the arterial pressure in moderate essential hypertension appears to facilitate the secretion and osmoregulation of AVP. On the other hand, during prolonged antihypertensive treatment, baroreflex regulation of the secretion of AVP appears to be set at a lower operating point, thus exerting the same influence on the release of AVP as it did before antihypertensive treatment.

Original languageEnglish
Pages (from-to)1277-1283
Number of pages7
JournalJournal of Hypertension
Volume15
Issue number11
DOIs
Publication statusPublished - 1997

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Osmoregulation
Vasopressins
Antihypertensive Agents
Hypertension
Arterial Pressure
Therapeutics
Clonidine
Nitroprusside
Hypertonic Solutions
Baroreflex
Drug Combinations
Intravenous Infusions
Pharmaceutical Preparations
Osmolar Concentration

Keywords

  • Baroreflexes
  • Hypertension
  • Osmoregulation
  • Vasopressin

ASJC Scopus subject areas

  • Endocrinology
  • Internal Medicine

Cite this

Effects of antihypertensive treatment on vasopressin secretion and on its osmoregulation in moderate hypertension. / Del Bo, Alberto; Suraci, Sandra; Giuditta, Marianna; Mistò, Martina; Zanchetti, Alberto.

In: Journal of Hypertension, Vol. 15, No. 11, 1997, p. 1277-1283.

Research output: Contribution to journalArticle

Del Bo, Alberto ; Suraci, Sandra ; Giuditta, Marianna ; Mistò, Martina ; Zanchetti, Alberto. / Effects of antihypertensive treatment on vasopressin secretion and on its osmoregulation in moderate hypertension. In: Journal of Hypertension. 1997 ; Vol. 15, No. 11. pp. 1277-1283.
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abstract = "Background. Changes in plasma osmolality and arterial pressure can affect the secretion of vasopressin (AVP). Objective. To investigate the effect of a drug-induced lowering of the arterial pressure on the plasma concentration of AVP and on its osmoregulation in moderately severe uncomplicated hypertensives. Design and methods. A group of 33 moderate uncomplicated and untreated essential hypertensives of both sexes (mean age 48 ± 1 years, average arterial pressure 171 ± 3/108 ± 2 mmHg) was studied. We measured AVP and other plasma and urine variables in 21 of them before and after administration of a hypertonic NaCl solution (100 mmol NaCl in 50 ml). Antihypertensive treatment with a single drug or, if necessary, with a combination of drugs was initiated for eight of these subjects and hypertonic saline administration was repeated after 1 month of treatment. The hypertonic stimulus was administered to the other 12 subjects after acute lowering of the arterial pressure by continuous intravenous infusion either of 0.3 mg clonidine in 100 ml (n = 6) or of 50 mg sodium nitroprusside in 250 ml (n = 6). Results. Administration of hypertonic saline to untreated hypertensives increased their AVP level from 1.6 ± 0.28 to 5.4 ± 0.7 pg/ml (n = 21, P <0.01). Their mean arterial pressure was lowered after pharmacological treatment for 1 month (n = 8) from 125 ± 2 to 101 ± 2 mmHg; their baseline AVP level remained unchanged (1.2 ± 0.21 versus 0.9 ± 0.25 pg/ml); after hypertonic saline had been administered to hypertensives with lowered arterial pressures, their AVP level increased to 6.0 ± 1.03 pg/ml (P <0.01). The AVP level in subjects whose MAP had been lowered acutely by administration of clonidine (n = 6) or of sodium nitroprusside (n = 6; on the average, from 132 ± 3 to 110 ± 4 mmHg) increased concurrently from 1.6 ± 0.63 to 3.4 ± 0.7 pg/ml (P <0.05); after administration of the hypertonic saline the AVP level increased to 10.8 ± 2.22 pg/ml (P <0.01). This stimulated value was significantly (P <0.01) higher than that observed after hypertonic saline had been administered to untreated hypertensives (5.4 ± 0.7 pg/ml). Conclusions. Acute lowering of the arterial pressure in moderate essential hypertension appears to facilitate the secretion and osmoregulation of AVP. On the other hand, during prolonged antihypertensive treatment, baroreflex regulation of the secretion of AVP appears to be set at a lower operating point, thus exerting the same influence on the release of AVP as it did before antihypertensive treatment.",
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T1 - Effects of antihypertensive treatment on vasopressin secretion and on its osmoregulation in moderate hypertension

AU - Del Bo, Alberto

AU - Suraci, Sandra

AU - Giuditta, Marianna

AU - Mistò, Martina

AU - Zanchetti, Alberto

PY - 1997

Y1 - 1997

N2 - Background. Changes in plasma osmolality and arterial pressure can affect the secretion of vasopressin (AVP). Objective. To investigate the effect of a drug-induced lowering of the arterial pressure on the plasma concentration of AVP and on its osmoregulation in moderately severe uncomplicated hypertensives. Design and methods. A group of 33 moderate uncomplicated and untreated essential hypertensives of both sexes (mean age 48 ± 1 years, average arterial pressure 171 ± 3/108 ± 2 mmHg) was studied. We measured AVP and other plasma and urine variables in 21 of them before and after administration of a hypertonic NaCl solution (100 mmol NaCl in 50 ml). Antihypertensive treatment with a single drug or, if necessary, with a combination of drugs was initiated for eight of these subjects and hypertonic saline administration was repeated after 1 month of treatment. The hypertonic stimulus was administered to the other 12 subjects after acute lowering of the arterial pressure by continuous intravenous infusion either of 0.3 mg clonidine in 100 ml (n = 6) or of 50 mg sodium nitroprusside in 250 ml (n = 6). Results. Administration of hypertonic saline to untreated hypertensives increased their AVP level from 1.6 ± 0.28 to 5.4 ± 0.7 pg/ml (n = 21, P <0.01). Their mean arterial pressure was lowered after pharmacological treatment for 1 month (n = 8) from 125 ± 2 to 101 ± 2 mmHg; their baseline AVP level remained unchanged (1.2 ± 0.21 versus 0.9 ± 0.25 pg/ml); after hypertonic saline had been administered to hypertensives with lowered arterial pressures, their AVP level increased to 6.0 ± 1.03 pg/ml (P <0.01). The AVP level in subjects whose MAP had been lowered acutely by administration of clonidine (n = 6) or of sodium nitroprusside (n = 6; on the average, from 132 ± 3 to 110 ± 4 mmHg) increased concurrently from 1.6 ± 0.63 to 3.4 ± 0.7 pg/ml (P <0.05); after administration of the hypertonic saline the AVP level increased to 10.8 ± 2.22 pg/ml (P <0.01). This stimulated value was significantly (P <0.01) higher than that observed after hypertonic saline had been administered to untreated hypertensives (5.4 ± 0.7 pg/ml). Conclusions. Acute lowering of the arterial pressure in moderate essential hypertension appears to facilitate the secretion and osmoregulation of AVP. On the other hand, during prolonged antihypertensive treatment, baroreflex regulation of the secretion of AVP appears to be set at a lower operating point, thus exerting the same influence on the release of AVP as it did before antihypertensive treatment.

AB - Background. Changes in plasma osmolality and arterial pressure can affect the secretion of vasopressin (AVP). Objective. To investigate the effect of a drug-induced lowering of the arterial pressure on the plasma concentration of AVP and on its osmoregulation in moderately severe uncomplicated hypertensives. Design and methods. A group of 33 moderate uncomplicated and untreated essential hypertensives of both sexes (mean age 48 ± 1 years, average arterial pressure 171 ± 3/108 ± 2 mmHg) was studied. We measured AVP and other plasma and urine variables in 21 of them before and after administration of a hypertonic NaCl solution (100 mmol NaCl in 50 ml). Antihypertensive treatment with a single drug or, if necessary, with a combination of drugs was initiated for eight of these subjects and hypertonic saline administration was repeated after 1 month of treatment. The hypertonic stimulus was administered to the other 12 subjects after acute lowering of the arterial pressure by continuous intravenous infusion either of 0.3 mg clonidine in 100 ml (n = 6) or of 50 mg sodium nitroprusside in 250 ml (n = 6). Results. Administration of hypertonic saline to untreated hypertensives increased their AVP level from 1.6 ± 0.28 to 5.4 ± 0.7 pg/ml (n = 21, P <0.01). Their mean arterial pressure was lowered after pharmacological treatment for 1 month (n = 8) from 125 ± 2 to 101 ± 2 mmHg; their baseline AVP level remained unchanged (1.2 ± 0.21 versus 0.9 ± 0.25 pg/ml); after hypertonic saline had been administered to hypertensives with lowered arterial pressures, their AVP level increased to 6.0 ± 1.03 pg/ml (P <0.01). The AVP level in subjects whose MAP had been lowered acutely by administration of clonidine (n = 6) or of sodium nitroprusside (n = 6; on the average, from 132 ± 3 to 110 ± 4 mmHg) increased concurrently from 1.6 ± 0.63 to 3.4 ± 0.7 pg/ml (P <0.05); after administration of the hypertonic saline the AVP level increased to 10.8 ± 2.22 pg/ml (P <0.01). This stimulated value was significantly (P <0.01) higher than that observed after hypertonic saline had been administered to untreated hypertensives (5.4 ± 0.7 pg/ml). Conclusions. Acute lowering of the arterial pressure in moderate essential hypertension appears to facilitate the secretion and osmoregulation of AVP. On the other hand, during prolonged antihypertensive treatment, baroreflex regulation of the secretion of AVP appears to be set at a lower operating point, thus exerting the same influence on the release of AVP as it did before antihypertensive treatment.

KW - Baroreflexes

KW - Hypertension

KW - Osmoregulation

KW - Vasopressin

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