The impaired fibrinolytic capacity in hypertension is unaffected by acute blood pressure lowering
Abstract
The endogenous fibrinolytic system and the ability of the endothelium to release tissue-plasminogen activator (t-PA) play a pivotal role to protect humans from atherothrombotic events. We have recently reported that the decreased capacity for t-PA release in hypertension is restored with chronic blood pressure lowering. Thus, we explored if acute blood pressure lowering has the same effect. The capacity for acute t-PA release was investigated in the perfused-forearm model during stimulation by intra-arterial substance P 8 pmol/min in hypertensive subjects. The procedure was then repeated during acute blood pressure lowering (n = 9) induced by sodium nitroprusside (SNP) infusion or during placebo infusion (n = 3). SNP lowered mean arterial pressure from 108.6 (2.6) to 83.0 (2.6) (mean and SEM) mmHg (P < 0.001). Substance P induced significant increase in t-PA release during both high- and low-pressure conditions (P < 0.01, ANOVA). Peak t-PA release rate was 199 (77) and 167 (41) (mean and SEM) ng/min/l tissue, and accumulated t-PA release was 2,395 (750) and 2,394 (473) ng, during high- and low-pressure conditions, respectively. t-PA release and hemodynamic responses were almost identical during high- and low-pressure conditions (P = ns, for all). Acute blood pressure lowering does not restore stimulated t-PA release from the endothelium in hypertensive subjects. These findings are in contrast to previously described effects of chronic blood pressure treatment. Although data need to be confirmed in a larger study, they suggest that high blood pressure decreases the cellular t-PA pool rather than interferes with release mechanisms of the protein.
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Endothelial t-PA release is diminished in obesity and in conditions associated with prediabetes, such as hypertension, but the effect of hyperglycemia is not well-defined.
“Endothelial t-PA release is diminished in obesity and in conditions associated with prediabetes, such as hypertension, but the effect of hyperglycemia is not well-defined.”
From The Vasculature in Prediabetes (2018) · cites this paper as [130]
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- Authors
- Ridderstråle, W., Saluveer, O., Carlström, M., Jern, S., & Hrafnkelsdóttir, T. J.
- Affiliations
- University of Gothenburg (SE)
- Sahlgrenska University Hospital (SE)
- Corresponding author
- Saluveer, Ott
- Venue
- Journal of Thrombosis and Thrombolysis
- Published
- 2011-05-26
- Volume
- 32
- Issue
- 4
- Pages
- 399-404
- ISSN
- 0929-5305 (ISSN-L)
- 1573-742X
- OpenAlex
- W1967008520
- Cited by
- 7
- References
- 24
- Citations by year
- 2025: 1 · 2021: 1 · 2018: 1 · 2017: 2 · 2014: 1 · 2012: 1
- FWCI
- 0.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Thrombosis and Thrombolysis (publishedVersion)
- PubMed (publishedVersion)
- Hirsla (Landspítali University Hospital) (submittedVersion)
- Funders
- Vetenskapsrådet
- Göteborgs Läkaresällskap
- Topics
- Health Sciences › Medicine › Hematology › Blood Coagulation and Thrombosis Mechanisms
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Blood properties and coagulation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Keywords
- hypertension, tissue plasminogen activator, fibrinolysis, sodium nitroprusside, substance P, atherothrombosis
- MeSH terms
- Antihypertensive Agents, Blood Pressure, Endothelium, Vascular, Fibrinolysis, Humans, Hypertension, Middle Aged, Nitroprusside, Tissue Plasminogen Activator, Substance P, Vasodilator Agents
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