Severely Impaired Baroreflex-Buffering in Patients With Monogenic Hypertension and Neurovascular Contact
| Autor: | Hermann Haller, Karsten Heusser, Jens Jordan, Ramin Naraghi, Mandy Stoffels, Okan Toka, Friedrich C. Luft, Jens Tank, Herbert Schuster, Hans P. Schobel, John R. Shannon, Christine Stabroth, Wolfgang Oelkers, Hakan R. Toka, André Diedrich |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Adult
medicine.medical_specialty Vasopressin Baroreceptor Adolescent Valsalva Maneuver Ganglionic Blockers Vasodilator Agents Posture Blood Pressure Pressoreceptors Baroreflex Fingers Phenylephrine Heart Rate Cerebellum Physiology (medical) Internal medicine medicine Humans Vasoconstrictor Agents Genes Dominant business.industry Cold pressor test Syndrome Cerebral Arteries Neurovascular bundle Magnetic Resonance Imaging Cold Temperature Electrophysiology Autonomic nervous system Endocrinology Blood pressure medicine.anatomical_structure Hypertension Cardiology Cardiology and Cardiovascular Medicine business Brain Stem Blood vessel |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1524-4539 0009-7322 |
| Popis: | Background —We identified a family with a monogenic syndrome of hypertension, brachydactyly, and neurovascular contact of the brain stem. Neurovascular contact of the ventrolateral medulla may lead to arterial hypertension by interfering with baroreflex function. Methods and Results —In 5 patients with monogenic hypertension (18 to 34 years old), we conducted detailed autonomic function tests. Blood pressure during complete ganglionic blockade was 134±4.9/82±4.1 mm Hg and 90±6/49±2.4 mm Hg in patients and in control subjects, respectively. During ganglionic blockade, plasma vasopressin concentration increased 24-fold in control subjects and Conclusions —In patients with monogenic hypertension and neurovascular contact, basal blood pressure was increased even during sympathetic and parasympathetic nerve traffic interruption. However, sympathetic stimuli caused an excessive increase in blood pressure. This excessive response cannot be explained by increased sympathetic nerve traffic or increased vascular sensitivity. Instead, we suggest that baroreflex buffering and baroreflex-mediated vasopressin release are severely impaired. |
| Databáze: | OpenAIRE |
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