# REGULATION OF TESTICULAR BLOOD FLOW

> **NIH NIH R01** · UNIVERSITY OF VIRGINIA · 1993 · $109,587

## Abstract

The proposed research will test the hypothesis that the steroidogenic and
spermatogenic functions of the hamster testis are controlled by vascular
mechanisms that modulate capillary perfusion, and thereby regulate the
supply-demand ratio for oxygen.  We assert that local vascular control
mechanisms are a significant determinant of Leydig cell (steroidogenesis)
and seminiferous tubule (spermatogenesis) performance because the cell
types responsible for these two functions are perfused via separate
capillary beds.  Each capillary bed is controlled by individual arterioles,
so the potential to regulate perfusion and, therefore, the performance of
the two functional cell types is great.  This proposition is supported by
a massive body of indirect evidence derived from biochemical and
physiological assessments of testicular function.  For example, bursts in
Leydig cell oxidative demand are triggered by the episodic discharge of
pituitary luteinizing hormone which stimulates oxygen dependent enzyme
reactions.  Surges in germ cell oxidative demand coincide with mitotic
and/or meiotic events that occur within well-defined segments (2-6 mm) of
seminiferous tubules.  We will test the proposition that vascular
regulatory processes intrinsic to the testis directly control
steroidogenesis or spermatogenesis by modulating the availability of
oxygen, tropic hormones, and substrates.  To our knowledge, no single
laboratory possessed the skills to assess simultaneously both the
functional status of testicular parenchymal cells and the vasomotor
regulation of capillary perfusion.  This special expertise has now been
assembled in our laboratory.  Using this expertise, we will examine
vasomotor responses and their influences on function when triggered by:  i)
restricted perfusion pressure or vascular inflow, ii) local metabolic
stimuli arising from the selective activation of Leydig cells or
seminiferous tubules, and iii) electrical stimulation of the spermatic
nerve.  Each stimulus will be examined to determine its potential to
regulate arteriolar tone, to limit or promote the differential perfusion of
the dual capillary beds, and to selectively alter the performance of Leydig
cells or the seminiferous epithilium in of adult hamsters.  The proposed
studies develop new concepts to explain the regulation of Leydig cell
function and spermatogenesis by mechanisms intrinsic to the terminal
vascular bed.  This work has special importance to human reproductive
health because it provides a framework for investigating the unknown
etiology of testicular vascular disorders (varicocele, orchitis, and
cryptorchidism), the most prominent source of testicular dysfunction and
infertility.

## Key facts

- **NIH application ID:** 2198114
- **Project number:** 5R01HD020876-04
- **Recipient organization:** UNIVERSITY OF VIRGINIA
- **SAM.gov UEI:** JJG6HU8PA4S5
- **Principal Investigator:** CLAUDE DESJARDINS
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1993
- **Award amount:** $109,587
- **Award type:** 5
- **Project period:** 1986-09-01 → 1995-02-28

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2198114

## Citation

> US National Institutes of Health, RePORTER application 2198114, REGULATION OF TESTICULAR BLOOD FLOW (5R01HD020876-04). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2198114. Licensed CC0.

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