English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

We investigated the hemodynamics of the greater and lesser circulation in 35 patients with primary hypertension, as well as the effects of calcium-channel blockade, to test whether a common factor may account for the excessive vascular resistance in the two circuits and whether intracellular calcium concentration ([Ca++]i) may be involved. We proved that (1) elevated pulmonary arteriolar resistance (PAR) is not related to pulmonary blood flow and volume, pleural pressure, arterial oxygen or carbon dioxide tension and pH, left ventricular filling pressure and function; (2) systemic vascular resistance (SVR) significantly correlates with PAR; (3) calcium-channel blockade with nifedipine reduces systemic and pulmonary arterial pressures toward normal and significantly lowers both SVR and PAR; (4) the percent decrease in vascular resistance after nifedipine is related to the baseline level of resistance in both the greater and the lesser circulations. Failure of the mechanisms currently indicated as responsible for pulmonary vasoconstriction to explain convincingly the increased PAR, the correlation between SVR and PAR, as well as the qualitatively similar response to calcium-channel blockade suggest that a common factor produces vasoconstriction in the two circuits. A pathogenetic role of a primary disorder in [Ca++]i cannot be excluded, but remains to be proved.

Evidence of a shared mechanism of vasoconstriction in pulmonary and systemic circulation in hypertension: a possible role of intracellular calcium.