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H1 blockers are a class of widely prescribed drugs, here an excerpt of its pharmacodynamics (Source: Katzung’s Basic and Clinical Pharmacology)

A. HISTAMINE-RECEPTOR BLOCKADE
H₁-receptor antagonists block the actions of histamine by reversible competitive antagonism at the H₁ receptor. They have negligible potency at the H₂ receptor and little at the H₃ receptor. For example, histamine-induced contraction of bronchiolar or gastrointestinal smooth muscle can be completely blocked by these agents, but the effects on gastric acid secretion and the heart are unmodified.

B. ACTIONS NOT CAUSED BY HISTAMINE RECEPTOR BLOCKADE
The first-generation H₁-receptor antagonists have many actions not ascribable to blockade of the actions of histamine. The large number of these actions probably results from the similarity of the general structure (Figure 16-1) to the structure of drugs that have effects at muscarinic cholinoceptor, a adrenoceptor, serotonin, and local anesthetic receptor sites. Some of these actions are of therapeutic value and some are undesirable.
1. Sedation A common effect of first-generation H₁ antagonists is sedation, but the intensity of this effect varies among chemical subgroups (Table 16-2) and among patients as well. The effect is sufficiently prominent with some agents to make them useful as “sleep aids” (see Chapter 64) and unsuitable for daytime use. The effect resembles that of some antimuscarinic drugs and is considered very unlike the disinhibited sedation produced by sedative-hypnotic drugs. Compulsive use has not been reported. At ordinary dosages, children occasionally (and adults rarely) manifest excitation rather than sedation. At very high toxic dose levels, marked stimulation, agitation, and even convulsions may precede coma. Second-generation H₁ antagonists have little or no sedative or stimulant actions. These drugs (or their active metabolites) also have far fewer autonomic effects than the first-generation antihistamines.
2. Antinausea and antiemetic actions Several first-generation H₁ antagonists have significant activity in preventing motion sickness (Table 16-2). They are less effective against an episode of motion sickness already present. Certain H₁ antagonists, notably doxylamine (in Bendectin), were used widely in the past in the treatment of nausea and vomiting of pregnancy (see below).

3. Antiparkinsonism effects Some of the H₁ antagonists, especially diphenhydramine, have significant acute suppressant effects on the extrapyramidal symptoms associated with certain antipsychotic drugs. This drug is given parenterally for acute dystonic reactions to antipsychotics.

4. Anticholinoceptor actions Many of the first-generation agents, especially those of the ethanolamine and ethylenediamine subgroups, have significant atropine-like effects on peripheral muscarinic receptors. This action may be responsible for some of the (uncertain) benefits reported for nonallergic rhinorrhea but may also cause urinary retention and blurred vision.

5. Adrenoceptor-blocking actions Alpha-receptor-blocking effects can be demonstrated for many H₁ antagonists, especially those in the phenothiazine subgroup, eg, promethazine. This action may cause orthostatic hypotension in susceptible individuals. Beta-receptor blockade is not observed.

6. Serotonin-blocking action Strong blocking effects at serotonin receptors have been demonstrated for some first-generation H₁ antagonists, notably cyproheptadine. This drug is promoted as an antiserotonin agent and is discussed with that drug group. Nevertheless, its structure resembles that of the phenothiazine antihistamines, and it is a potent H₁-blocking agent.

7. Local anesthesia Several first-generation H₁ antagonists are potent local anesthetics. They block sodium channels in excitable membranes in the same fashion as procaine and lidocaine. Diphenhydramine and promethazine are actually more potent than procaine as local anesthetics. They are occasionally used to produce local anesthesia in patients allergic to conventional local anesthetic drugs. A small number of these agents also block potassium channels; this action is discussed below.

8. Other actions Certain H₁ antagonists, eg, cetirizine, inhibit mast cell release of histamine and some other mediators of inflammation. This action is not due to H₁-receptor blockade. The mechanism is not understood but could play a role in the beneficial effects of these drugs in the treatment of allergies such as rhinitis. A few H₁ antagonists (eg, terfenadine, acrivastine) have been shown to inhibit the P-glycoprotein transporter found in cancer cells, the epithelium of the gut, and the capillaries of the brain. The significance of this effect is not known.

There is also a related post on histamine physiologic effects.