P4.27 AUTONOMIC NERVOUS SYSTEM REACTIVITY IN NORMOTENSIVE SUBJECTS WITH A FAMILY HISTORY OF HYPERTENSION DURING VALSALVA MANOEUVRE

Abstract Background Syncope commonly results in emergency room and physician visits, leading to hospitalization and invasive investigations. Up to 24% of these presentations may be caused by neurogenic orthostatic hypotension (nOH), which continues to be an under-recognized clinical entity. We review an approach to diagnosing nOH. Case summary An 85-year-old man with a history of Parkinson’s disease was referred for a history of recurrent syncope, which had resulted in extensive cardiac investigation. Collateral history revealed that the events were orthostatic in nature, but with variable time to onset of symptoms. The patient was found to have significant postural drop in blood pressure without compensatory tachycardia. Cardiovascular autonomic function testing was performed, which confirmed significant autonomic nervous system failure, including a marked hypotensive response on tilt-table testing and a lack of vasoconstriction during Valsalva manoeuvre. The patient was diagnosed with nOH and initiated on midodrine with subjective improvement in the frequency of syncope. Discussion Autonomic nervous system failure, with nOH, is a common cause of recurrent syncope, particularly in older patients. Attention to detail during the medical history, including precipitating factors and the presence of prodromal symptoms prior to syncope, is critical for making the correct diagnosis. Measuring orthostatic vital signs correctly in patients with syncope provides valuable information, is cost-effective, and critical to diagnose nOH.

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Whole-blood viscosity, autonomic nervous system, and effects of mental stress in borderline hypertensive and normotensive subjects

American Journal of Hypertension ◽

10.1016/j.amjhyper.2004.03.031 ◽

2004 ◽

Vol 17 (5) ◽

pp. S14-S15

Author(s):

H REIMS

Keyword(s):

Nervous System ◽

Autonomic Nervous System ◽

Blood Viscosity ◽

Whole Blood ◽

Mental Stress ◽

Whole Blood Viscosity ◽

Autonomic Nervous ◽

Normotensive Subjects

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ACTIVITY OF AUTONOMIC NERVOUS SYSTEM AND MICROVASCULAR REACTIVITY IN NORMOTENSIVE SUBJECTS WITH A FAMILIAL PREDISPOSITION TO HYPERTENSION

Journal of Hypertension ◽

10.1097/00004872-200006001-00265 ◽

2000 ◽

Vol 18 ◽

pp. S81

Author(s):

J. Maver ◽

M. Štrucl ◽

R. Accetto

Keyword(s):

Nervous System ◽

Autonomic Nervous System ◽

Familial Predisposition ◽

Microvascular Reactivity ◽

Autonomic Nervous ◽

Normotensive Subjects

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Failure of angiotensin II to suppress plasma renin activity in normotensive subjects with a positive family history of hypertension

Clinical Science ◽

10.1042/cs20050055 ◽

2005 ◽

Vol 109 (3) ◽

pp. 311-317 ◽

Cited By ~ 1

Author(s):

Hans Herlitz ◽

Eva Palmgren ◽

Bengt Widgren ◽

Mattias Aurell

Keyword(s):

Angiotensin Ii ◽

Family History ◽

Plasma Renin Activity ◽

Plasma Renin ◽

Urinary Sodium ◽

Renin Activity ◽

Ang Ii ◽

History Of ◽

Family History Of Hypertension ◽

Normotensive Subjects

The renin–angiotensin system is implicated in the pathophysiology of hypertension. Renin release is regulated by a number of factors, including circulating Ang II (angiotensin II), the so-called short feedback loop. The aim of the present study was to investigate the responsiveness of circulating Ang II on PRA (plasma renin activity) in normotensive subjects with a PFH or NFH (positive or negative family history of hypertension respectively). PRA, renal haemodynamics and urinary sodium excretion were measured during infusion of Ang II without and with pretreatment with the AT1 (Ang II type 1) receptor blocker irbesartan. Normotensive men with a PFH (n=13) and NFH (n=10), with a mean age of 38 years, were given on different occasions intravenous Ang II infusions of 0.1, 0.5 and 1.0 ng·kg−1 of body weight·min−1 before and after pretreatment with 150 mg of irbesartan once a day for 5 consecutive days. RPF (renal plasma flow) and GFR (glomerular filtration rate) were also measured. Before Ang II infusion, the PFH and NFH groups did not differ with respect to BP (blood pressure), body mass index, PRA, RBF (renal blood flow) or urinary sodium. There was no difference in BP or renal haemodynamic response to the highest Ang II dose between the groups. PRA declined with the highest Ang II dose (P<0.01) in subjects with a NFH, but not in subjects with a PFH. After treatment with irbesartan when Ang II had no effect on BP in either group, Ang II also suppressed PRA in subjects with a PFH (P<0.01), and the difference between the groups at baseline was thus eliminated. In conclusion, these findings indicate that subjects with a PFH have a defective Ang II suppression of PRA, which is corrected by AT1 receptor blockade.

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Intracellular Na+ and Ca2+ Activities in Essential Hypertension

Clinical Science ◽

10.1042/cs063041s ◽

1982 ◽

Vol 63 (s8) ◽

pp. 41s-43s ◽

Cited By ~ 36

Author(s):

W. Zidek ◽

H. Vetter ◽

K.-G. Dorst ◽

H. Zumkley ◽

H. Losse

Keyword(s):

Essential Hypertension ◽

Family History ◽

Secondary Hypertension ◽

Genetic Trait ◽

Hypertensive Patients ◽

Intracellular Na Activity ◽

History Of ◽

Family History Of Hypertension ◽

Normotensive Subjects

1. The intracellular Na+ and Ca2+ activity and Na+ concentration were measured in erythrocytes of normotensive subjects, with and without a familial disposition to hypertension, in essential hypertensive patients with and without a family history of hypertension, and in patients with secondary hypertension. 2. In normotensive subjects without a genetic trait of hypertension intracellular Na+ activity and concentration were 7.00 ± 1.38 mmol/l and 5.67 ± 0.95 mmol/l respectively. The intracellular Ca2+ activity was 4.82 ± 4.49 μmol/l. In normotensive subjects with a familial hypertensive disposition intracellular Na+ activity and concentration were 9.74 ± 1.43 mmol/l (P < 0.01) and 6.63 ± 0.88 mmol/l (P < 0.05). Intracellular Ca2+ was 9.59 ± 9.71 μmol/l (P < 0.05). 3. Essential hypertensive patients without a familial genetic trait had an elevated intracellular Na+ activity (8.35 ± 2.08 mmol/l, P < 0.05). Intracellular Na+ concentration was 6.64 ± 0.79 mmol/l (P < 0.05). The intracellular Ca2+ activity was markedly elevated to 25.33 ± 19.03 μmol/l (P < 0.01). The essential hypertensive patients with a familial disposition had an elevated intracellular Na+ activity (17.19 ± 4.37 mmol/l, P < 0.001) and Ca2+ activity (32.8 ± 32.51 μmol/l, P < 0.01). The intracellular Na+ concentration was 6.25 ± 1.23 mmol/l. 4. The results indicate that in essential hypertension intracellular Na+ activity is increased, particularly in patients with a familial disposition for hypertension. Intracellular Ca2+ is increased in essential hypertension whether or not there was a family disposition to hypertension.

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