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1 Department of Experimental Medical Science, Lund University, Lund, Sweden
2 Department of Experimental medical science, Lund University, Lund, Skane, Sweden
3 Department of Nephrology, Lund University, Lund, Sweden
4 Dept of Nephrology, Lund University, Lund, Sweden; Department of Biomedicine, Section for Physiology, University of Bergen, Jonas Lies Vei 91, Bergen, N-5009, Norway
5 Dept of Nephrology, Lund University, Lund, Sweden
6 Institute for Physiological Chemistry and Pathobiochemistry, University of Munster, Munster, Germany
7 Dept. of Experimental Medical Science, Lund University, Lund, Sweden
8 Department of Nephrology, University Hospital of Lund, Lund, Sweden
9 Department of Experimental Medical Science, University of Lund, Lund, Sweden
* To whom correspondence should be addressed. E-mail: Karl.Sward{at}med.lu.se.
Caveolin-1 (Cav-1) is essential for the morphology of membrane caveolae and exerts a negative influence on a number of signaling systems, including NO production and activity of the MAP kinase cascade. In the vascular system, ablation of caveolin-1 may thus be expected to cause arterial dilatation and increased vessel wall mass (remodeling). This was tested in Cav-1 knockout (KO) mice by a detailed morphometric and functional analysis of mesenteric resistance arteries, shown to lack caveolae. Quantitative morphometry revealed increased media thickness and media-to-lumen ratio in KO. Pressure-induced myogenic tone and flow-induced dilatation were decreased in KO arteries, but both were increased towards wild-type (WT) levels following nitric oxide synthase (NOS) inhibition. Isometric force recordings following NOS inhibition showed rightward shifts of passive and active length-force relationships in KO, and the force response to 
1-adrenergic stimulation was increased. In contrast, media thickness and force response of the aorta were unaltered in KO vs. WT, whereas lumen diameter was increased. Mean arterial blood pressure during isoflurane anesthesia was not different in KO vs. WT, but greater fluctuation in blood pressure over time was noted. Following NOS inhibition fluctuations disappeared and pressure increased twice as much in KO (38±6%) compared to WT (17±3%). Tracer dilution experiments showed increased plasma volume in KO. We conclude that NO affects blood pressure more in Cav-1 KO than in WT mice and that restructuring of resistance vessels and an increased responsiveness to adrenergic stimulation compensate for a decreased tone in Cav-1 KO mice.
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